KeywordsCatheter malfunction, Chyloperitoneum, Dialysate leak, Drain pain, Encapsulating peritoneal sclerosis, Hemoperitoneum, Hernia formation, Hydrothorax, Metabolic complications, Peritoneal dialysis
Complications Related to Increased Intraabdominal Pressure, 520
Malfunction of the Peritoneal Catheter, 527
Drain Pain, 528
Metabolic Complications, 531
Lipid Abnormalities, 531
Insulin Resistance, 531
Hepatic Subcapsular Steatosis, 531
Electrolyte Disorders, 532
Encapsulating Peritoneal Sclerosis, 532
Prevention of Encapsulating Peritoneal Sclerosis, 537
Encapsulating Peritoneal Sclerosis and Renal Transplantation, 537
Although peritonitis is regarded as the Achilles heel of peritoneal dialysis (PD), a number of serious noninfectious complications can develop in patients on PD. These complications can lead to significant morbidity and mortality. Some complications, such as catheter malfunction, hernias, and dialysate leaks, are commonly encountered; others, such as encapsulating peritoneal sclerosis, are rare and can be devastating ( Table 33.1 ). This chapter will address these and other noninfectious complications of PD.
|Early (d, wk)||Late (mo)|
|Catheter malfunction |
Displacement, kink, omental wrap
|Leak (<30 d) |
Usually at exit site or pericatheter (positive result when glucose test strip dipped in exit-site fluid)
|Leak (usually within first year) |
Leak through defect in peritoneum e.g., into an abdominal hernia or through a patent processus vaginalis
|Drain pain |
Often worse on cycler
|Encapsulating peritoneal sclerosis |
Major risk factor = long peritoneal dialysis vintage
Likely congenital diaphragmatic defect
Likely acquired diaphragmatic defect, sometimes presents coincident with peritonitis
Complications Related to Increased Intraabdominal Pressure
The instillation of dialysate into the peritoneal cavity leads to an increase in intraabdominal pressure (IAP). Two principal factors govern the magnitude of the rise in IAP: the volume of dialysate instilled and the position the patient assumes during the dwell. A strong positive relationship exists between the amount of dialysate instilled into the peritoneal cavity and IAP. The effect of patient position is also important, with the supine position generating the lowest IAP for a given volume of dialysate. Other factors that may increase IAP include higher body mass index (BMI) and activities such as exercising, coughing, and straining.
In accordance with Laplace law, the tension on the abdominal wall increases with instillation of dialysate as a result of the increase in IAP and the larger radius of the abdomen. High abdominal pressure and abdominal wall tension place mechanical stress on the supporting structures of the abdomen and can lead to hernia formation in those with congenital or acquired weakness or defects. The areas of weakness are probably very important in the pathogenesis of hernias.
Incidence, Types of Hernia, and Etiological Factors
The prevalence of hernia in PD patients has been reported to range from 10% to 25%. This is higher than in the general population. , The true prevalence of this condition may, in fact, be even higher due to the presence of asymptomatic hernias that are not detected until a complication occurs.
Umbilical hernias are the most commonly described hernia occurring in PD patients ( Fig. 33.1 ). However, a multitude of other types of hernia have been reported. These include incisional hernia, hiatal hernia, inguinal hernia, ventral hernia, epigastric hernia, femoral hernia, Spigelian hernia, cystocele, Richter hernia, and herniation through the foramen of Morgagni. , ,
Numerous risk factors for hernia formation exist, including older age, female sex, multiparity, midline PD catheter insertion, and having undergone a previous hernia repair ( Table 33.2 ). Moreover, some studies have demonstrated a correlation with an increased BMI, whereas others have reported the opposite effect. , , Continuous ambulatory peritoneal dialysis (CAPD), rather than night-cycler–based dialysis, has been reported as a risk factor for hernia, possibly as the result of an increased duration of time spent upright leading to sustained increased IAP. In addition, hernias are more common in patients who have previously undergone transplantation. Interestingly, they are generally not associated with the transplant incision and it is thought they may be related to chronic steroid use or changes in abdominal musculature.
|Large dialysate volumes|
|Raised intraabdominal pressure (during activities, e.g, exercise)|
|Recent abdominal surgery|
|Congenital anatomical defects|
|Polycystic kidney disease|
Finally, polycystic kidney disease can predispose PD patients to hernia development through multiple mechanisms, including higher IAP caused by the enlarged kidneys, a patent processus vaginalis, or as a manifestation of a generalized connective tissue disorder leading to weakening of the abdominal wall. , However, the theory that increased IAP caused by PD results in increased hernia risk is controversial with studies demonstrating conflicting results. ,
Clinical Presentation and Diagnosis
Typically, hernias present as a painless swelling. This may occur after an antecedent event such as a coughing bout or after physical exertion. Some hernias may be clinically occult and present with diminished effluent return or abdominal edema resulting from dialysate leak through defects in the abdominal wall. The most worrisome complications of hernia are incarceration and strangulation of bowel, which occurs most commonly with umbilical hernias. Patients may present with a tender lump, recurrent episodes of peritonitis with multiple gram-negative organisms, and signs and symptoms of bowel obstruction.
Diagnosing hernia usually is straightforward in the clinical setting. However, other tests may be needed to confirm the diagnosis. Ultrasonography is an excellent modality to distinguish pericatheter hernias from masses caused by hematomas, seromas, or abscesses. With ultrasound, hernias often appear solid, whereas the other conditions are characterized by fluid collections.
Although ultrasound is helpful in detecting pericatheter hernias, computed tomography (CT) is the most sensitive and specific modality to delineate other hernias. The diagnostic utility of the CT is improved by the use of intraperitoneal dye. Typically, 100 mL of dye is added to the dialysate, which is infused into the peritoneal cavity. The patient should remain ambulatory over the next 2 hours to facilitate the entry of peritoneal fluid containing the dye into the hernia sac and any other potential areas of leak. CT is then performed ( Fig. 33.2 ).
Magnetic resonance imaging (MRI) also has been used to diagnose hernias associated with abdominal wall and genital leaks. This modality is beneficial in that dialysate is used as the “dye,” thereby making it devoid of ionizing radiation. Furthermore, MRI will detect where dialysate is residing in the soft tissues, whereas CT will only pick up what has leaked following instillation of the dye.
The vast majority of patients on PD who develop a hernia should undergo surgical repair. A notable exception is those individuals who are an unacceptably high surgical risk. In these patients, however, the development of a hernia does not necessarily obviate the use of PD. In fact, PD may be continued if the patient uses methods to lower IAP such as dialysis while supine (night-cycler treatment), lower dialysate volumes, and wearing an abdominal binder for external support. Although hernias may be cosmetically unappealing, most should be repaired to prevent the serious complications of bowel incarceration and strangulation and to avoid the development of dialysate leaks. The risk for bowel incarceration and strangulation is particularly important for smaller umbilical hernias. In contrast, ventral hernias carry little risk for strangulation. However, the defect in the abdominal wall integrity associated with these hernias serves as a source of dialysate leak leading to the formation of abdominal edema.
Hernia repair sometimes incorporates a preperitoneal mesh placement. This allows development of an inflammatory state around the mesh, which helps to seal the peritoneal cavity. For a patient who has not yet initiated dialysis, hernia repair can occur at the same time as PD catheter insertion.
Reports have demonstrated that PD patients undergoing hernia repair need not be automatically converted to hemodialysis (HD) around the surgery. , These patients can continue standard PD therapy until the morning of surgery, drain the PD fluid before surgery, and withhold dialysis for the first 24 to 48 hours after surgery. Dialysis can then be safely reintroduced using the principles of low IAP (low volumes using a night-cycler and day dry) for a 2-week duration particularly in patients who have significant residual kidney function. Temporary transfer to HD should be initiated when the hernia is associated with bowel strangulation, which may compromise the bacterial barrier of the bowel wall and subject the patient to peritonitis. In the patient without renal kidney failure, it may be prudent to consider temporary support with HD. An example of a management strategy for PD before and after hernia surgery is outlined in Table 33.3 .
Previously, there was concern regarding the potential for mesh infection in patients on PD, although there is no compelling evidence for this. Generally, mesh infection rates are assumed to be higher in patients treated with intraperitoneal mesh (with exposure of the mesh to the peritoneal cavity) compared with preperitoneal mesh (with minimal breach of the peritoneum). Regardless, numerous published reports of mesh hernia repairs in PD patients report no episodes of mesh infection even in the presence of peritonitis.
Recurrence of surgically repaired hernias in PD patients has been reported to be as high as 27%, , although a more recent study (primarily using mesh repairs) was around 10%. In the event of recurrence, a long-term option for those on CAPD would be to switch to overnight ambulatory peritoneal dialysis (APD). A 2012 retrospective study evaluated the effect of hernia repair in PD patients over a 10-year period. Repair was done in 49 of 73 hernias (mainly umbilical). There was no significant effect on residual kidney function or technique survival with 86% of patients remaining on PD long-term.
The loss of dialysate from the peritoneal cavity, either into another compartment or around the PD catheter itself, is known as a peritoneal dialysate leak. This phenomenon often is a consequence of the loss of peritoneal membrane integrity caused by a defect within the membrane. It may manifest with a wide spectrum of presentations: from moisture around the PD catheter exit site to genital and abdominal wall edema. The ramifications of dialysate leaks can be distressing as they may lead to technique failure.
Incidence, Classification of Leaks, and Risk Factors
The incidence of dialysate leaks varies widely in the literature. Conservative reports demonstrate an incidence of 5% in PD patients; however, others have noted rates as high as 10%. , The variability in incidence may be the result of heterogeneity in the reporting of leaks. Dialysate leaks may be classified as early or late depending on the time course they develop after PD catheter insertion ( Table 33.4 ). Early leaks are those that develop within 30 days of catheter insertion. , They are usually related to catheter placement and present as dialysate leakage at the exit site or incision. In contrast, late leaks most often are related to a defect in the peritoneal membrane. , These leaks more often present with hydrothorax and genital and abdominal wall edema, sometimes in association with hernias.
|Early Leaks||Late Leaks|
The risk factors for the development of leaks are similar to those for hernia development. However, early leaks can be the result of not placing a secure purse-string suture around the deep cuff of the catheter. In addition, initiating dialysis too soon after catheter placement may increase the likelihood of a leak. A recent randomized controlled trial analyzed the appropriate time to initiate PD after catheter insertion. The trial randomized 122 patients to one of three groups: commencing PD at 1 week postcatheter insertion, at 2 weeks, or at 4 weeks. Catheter leak was significantly higher in the first group than in the third group (28.2% vs. 2.4%) but not compared with those waiting 2 weeks.
Complications of Dialysate Leaks
Genital edema occurs in 4% to 10% of PD patients. , Two mechanisms have been proposed to explain the formation of genital edema. First, dialysate can track through a patent processus vaginalis into the labia or scrotum, leading to a hydrocele composed of dialysis fluid. Along with dialysate, bowel also can migrate along the processus vaginalis into the scrotum, leading to a concurrent and often occult indirect inguinal hernia. The second mechanism leading to genital edema is imparted by defects in the abdominal wall, particularly at the catheter insertion site. These defects allow dialysate to track inferiorly along the abdominal wall, leading to edema of the mons pubis, scrotum, and foreskin (see Fig. 33.2 ). Women have a lower incidence of genital edema, which has been attributed to the processus vaginalis being patent more often in males due to the spermatic cord.
The diagnosis is usually obvious, but it is important to rule out other processes that may lead to similar presentations such as epididymitis or more generalized fluid overload. CT is the modality of choice to delineate the cause of the genital edema. The technique is similar to that used for the detection of hernias with dye being instilled into the peritoneal cavity with the dialysate. The subsequent scan, if positive, will show the movement of dialysate through a patent processus vaginalis or abdominal wall defect into the scrotum or labia ( Fig. 33.3 ). Radionuclide scanning also may be used.
The initial steps in the management of genital edema should address the risk factors leading to fluid accumulation. Specifically, measures aimed at decreasing IAP and minimizing fluid translocation along low-resistance pathways, such as the processus vaginalis, should be undertaken. In this regard, a conservative approach is used, which involves the discontinuation of CAPD, bed rest, scrotal elevation, and the initiation of continuous cyclic peritoneal dialysis (CCPD) or nocturnal intermittent peritoneal dialysis using low volumes with the patient supine. This is done for approximately 1 to 3 weeks. The success of this approach is usually dependent on having adequate residual renal function to compensate for the decrease in dose of PD. If the patient does not have adequate residual renal function, they should receive HD temporarily while waiting for the edema to dissipate and surgical repair of the defect. One center’s experience with this approach noted only a 14% rate of recurrence of genital edema.
If conservative treatments fail, surgical repair can be undertaken. In these cases, the same preoperative and postoperative principles as hernia repair apply.
Abdominal Wall Edema
The incidence of abdominal wall edema is not well defined in the literature; however, it is believed to occur less frequently than hernias. The presence of abdominal wall edema suggests that the origin of the peritoneal defect is located within one of the following sites: the incisional site for the insertion of the PD catheter, the catheter tunnel and exit site, from a soft tissue defect within a hernia ( Fig. 33.4 ), or from a peritoneal-fascial defect.
Abdominal wall edema may be difficult to detect clinically because it may present with nonspecific signs and symptoms. These include diminished effluent returns and weight gain due to dialysate accumulating in tissues of the abdominal wall. Other presenting features include abdominal asymmetry or increased abdominal girth. Patients with suspected abdominal wall edema should be examined while standing to better detect any abdominal asymmetry.
CT peritoneography or radionuclide scanning can be used for diagnostic purposes. MRI scanning also has been used, with one study revealing better delineation of dialysate movement than with CT. This finding is likely because MRI will detect dialysate residing in soft tissue, whereas CT will only detect dialysate that has leaked over the course of the study.
The principles of management of abdominal wall edema are similar to those of genital edema (see previous discussion). In brief, the dialysis regimen is converted to CCPD in the supine position with low volumes and a dry day. The goal is to allow the abdominal wall defect to heal on its own. Should this fail to occur, surgical intervention to close the defect is undertaken. If the leak is from a hernia, the hernia should be repaired.
Typically, pericatheter leaks are clinically obvious, presenting as wetness around the catheter exit site, or wetness of the exit-site dressing. The diagnosis can be proven using similar CT techniques as for hernias, genital, and abdominal wall edema. ,
The treatment of these leaks differs from that for abdominal wall and genital edema. Here the patient should be drained of dialysate and PD should be discontinued for at least 48 hours. Sometimes this yields enough time for the leak to seal; however, should this not be the case, then the patient should commence HD for a few days if dialysis is needed. If this fails to allow enough time for the leak to seal, then the catheter should be removed and reinserted at a different site. Overall, leaks have required catheter replacement in 37% to 48% of patients. Other interventions aimed at sealing the leak, including the placement of purse-string sutures or fibrin glue around the cuff after the fact have not been efficacious. A stitch should never be placed at the exit site. The source of the leak is where the catheter exits the peritoneal cavity, so exit-site stitches will only mask the problem and pose a risk for exit site infection.
Although dialysate leak at the exit site increases the risk for peritonitis or tunnel infection, the use of prophylactic antibiotics is usually not warranted unless there are signs of obvious infection.
Prevention of Dialysate Leaks
As previously discussed, there is evidence that delaying PD initiation for 2 weeks after catheter insertion can reduce the risk of a leak developing. It is important to use low volumes of dialysate if PD is to be initiated after a short or no break-in period to reduce the risk for pericatheter leakage. Similarly to hernia risk, failed transplant patients are probably at increased risk for leak presumably secondary to a long history of corticosteroid (CCS) use. Steroid use should be minimized where possible and sirolimus discontinued as long as possible before PD catheter insertion.
There is a growing interest in “acute-start” PD wherein a patient needing to start dialysis undergoes PD catheter insertion, avoiding exposure to a tunneled HD venous line. PD is started 1 or 2 days after PD catheter insertion, sooner than is typical for elective PD starts. Despite the increased incidence of leaks with this approach, patients rarely endure significant consequences and the vast majority do not need to transfer to HD.
Increased IAP can lead to the translocation of dialysate from the peritoneal cavity across the diaphragm and into the pleural space. The accumulation of dialysis fluid in the pleural space is called hydrothorax ( Fig. 33.5 ). This complication can occur almost immediately or as a late leak.
The pathogenesis of hydrothorax formation in PD patients has not been clearly elucidated. It has been speculated that two factors, possibly occurring concurrently, may be involved in hydrothorax development: (1) diaphragmatic defects combined with a large pleuroperitoneal pressure gradient and (2) abnormalities in lymphatic drainage.
Diaphragmatic Defects Combined with a Pleuroperitoneal Gradient
To allow the flux of dialysis fluid from the peritoneal cavity into the pleural space, a defect in the diaphragm, acting as a source of communication between the two spaces, must be present. However, it is not enough to have a defect; a pressure gradient also must exist between the two compartments to create a driving force for the movement of fluid. Higher IAP created by the instillation of dialysate combined with the negative pressure in the pleural space leads to a pressure gradient favoring fluid movement from the peritoneum into the pleura. Fluid will continue to move into the pleural space until there is equalization of pressure between the two compartments or there is an impediment to further movement. It has been postulated that a valve-like defect in the diaphragm or the action of the hepatic capsule to tamponade backflow of dialysate from the pleural to peritoneal space may be such impediments.
Other than a peritoneal-pleural gradient, one or multiple defects in the diaphragm must be present to allow hydrothorax formation. These defects may be congenital or acquired. The nature of the underlying defect may explain why some individuals develop hydrothorax with their first-ever infusion of dialysis fluid. Coughing and stretching of the diaphragm are common causes of pleural defects raising IAP to 120 to 150 mmH 2 O compared with “normal” baseline pressures of 0.5 to 2.2 mmH 2 O. The presence of PD fluid raises IAP to 2 to 10 cmH 2 O.
From a pathological point of view, it has been noted that anomalies in the formation of the diaphragm can lead to defects and herniations of this structure. Autopsy studies have revealed localized absence of muscle fibers in the hemidiaphragm, which are replaced with a disordered network of collagen. This collagen network is more susceptible to rupture when exposed to high pressures such as those provided by the instillation of dialysate. Moreover, when hydrothorax has been investigated by surgery, “blisters” or “blebs” have sometimes been noted on the pleural surface of the diaphragm. With the instillation of dialysate into the peritoneal cavity, these blebs can be seen to swell and even rupture, thus providing a pathway to the movement of fluid.
Patients presenting with hydrothorax months to years after PD initiation probably have an acquired defect of the diaphragm. Their attenuated diaphragmatic tissue is likely the consequence of ongoing injury from repeated exposure to raised IAP or recurrent episodes of peritonitis.
Abnormalities in Lymphatic Drainage or the Lymphatic Transfer Theory
The Lymphatic Transfer Theory was proposed to explain the contribution of impaired lymphatic drainage to the formation of hydrothorax in PD patients. Based on surgical findings, this theory suggests that in susceptible individuals, the instillation of dialysis fluid leads to engorgement of the phrenic lymphatic system resulting in the transudation of fluid into the pleural space. Although plausible, this mechanism cannot explain all cases of hydrothorax formation.
Incidence and Risk Factors
The incidence of hydrothorax in patients receiving PD has been reported to be 2%. Similar to hernias, it has been speculated that this figure is an underrepresentation of the true incidence of hydrothorax as the result of asymptomatic cases.
Multiple risk factors for the development of hydrothorax in PD patients have been described in the literature. However, it is interesting to note that in most cases of hydrothorax, a risk factor is not identified.
Polycystic kidney disease (PCKD) has been consistently associated with hydrothorax formation. Two potential explanations for this correlation are (1) the polycystic kidneys compound the rise in IAP when dialysate is infused into the peritoneal cavity, and (2) there is a greater inherent weakness of the diaphragm as a part of a generalized connective tissue defect seen in this condition.
Another important risk factor for hydrothorax is peritonitis. Although the link between these two conditions is not clear, it has been postulated that peritonitis may contribute to the further weakening of attenuated diaphragmatic tissue, thereby making it more susceptible to increases in IAP. Women are more likely than men to develop hydrothorax. The reason for this sexual predominance is unknown, although stretching of the hemidiaphragm from previous pregnancy contributing to its weakness has been suggested.
Most commonly, patients with PD-associated hydrothorax present with increasing shortness of breath. Other reported symptoms include pleuritic chest pain, diminished effluent volume, and weight gain as a result of decreased ultrafiltration. The use of hypertonic solutions often can make the situation worse due to increased ultrafiltration and greater IAP.
Moreover, as previously mentioned, it is not uncommon for hydrothorax to be clinically silent and only discovered incidentally during radiographic procedures done for some other reason.
It is interesting to note that the vast majority of hydrothoraces occur on the right side. One possible explanation for this predisposition has been attributed to cardiac and pericardial surfaces providing a protective effect by covering diaphragmatic defects on the left.
In the correct clinical setting, the diagnosis of hydrothorax in PD patients may be quite simple to make. Having said that, it is important to consider other causes of dyspnea in PD patients including congestive heart failure, parenchymal lung disease, and pulmonary embolism. Physical findings are consistent with pleural effusion and include absent breath sounds and stony dullness to percussion in the base of the affected lung. Chest x-ray demonstrates a pleural effusion that is usually right-sided and layers out when the patient is placed in the decubitus position. The clinical scenario wherein a patient develops a large right-sided pleural effusion within the first few dialysis exchanges is strongly suggestive of hydrothorax.
Historically, thoracentesis with pleural fluid analysis has been the first step in the diagnosis of PD-associated hydrothorax. As the pleural fluid is composed of dialysate, it should possess the same biochemical characteristics. That is, it should be a transudate, have a low lactic acid dehydragenase, and have a low white blood cell count. Because the glucose concentration in the dialysate solution is very high, the pleural glucose concentration in the hydrothorax should similarly be elevated; this diagnostic tool has led to the term sweet hydrothorax. Typically, a pleural fluid glucose concentration 50 mg/dL greater than serum glucose concentration is 100% sensitive and specific for diagnosing PD associated hydrothorax. However, cases with borderline glucose values are not uncommon. This may occur if the fluid has been left in the pleural cavity for many hours and is partially reabsorbed by the parietal lymphatics.
Another instance in which the pleural fluid may not have elevated glucose concentration is if the patient is using icodextrin for the long dwell. The presence of icodextrin in a pleural effusion can be demonstrated by the addition of iodine to a pleural fluid sample. This complexes with the starch resulting in a blue/black discoloration.
Instillation of methylene blue into the dialysate has been used in the past with subsequent pleural fluid analysis yielding a blue color. However, this is no longer recommended due to reports of a chemical peritonitis from this agent.
Radiological techniques used include scintigraphy, CT peritoneography, and MR peritoneography. Studies comparing techniques have generally had small numbers of patients. Peritoneal scintigraphy uses technetium-99m tagged macroaggregated albumin or sulfur colloid that is instilled into the peritoneal cavity with dialysate. It is a simple, noninvasive technique with low radiation exposure but has sensitivity rates of only 40% to 50%. In addition, although scintigraphy can provide evidence of a leak, the precise location of a defect is not demonstrated. Kang and Kim described the benefits of CT peritoneography, which has the additional benefit of locating the defect. They used 1 mL/kg of nonionic contrast mixed with 30 mL/kg of dialysate. After 30 to 60 minutes of ambulation, CT images can be taken. Sometimes a delayed scan may be warranted, particularly if the defect is small and fluid translocation time is long. MRI also has been used; it provides detailed information but without the radiation risk.
Before commencement of definitive treatment, immediate treatment of hydrothorax must be undertaken if there is respiratory compromise. This involves an emergent thoracentesis, which often dramatically improves the patients’ symptoms and provides pleural fluid for analysis.
Subsequent treatment is dictated by whether the patient chooses to continue on PD. If the patient wants to transfer to HD, further management is not required once the effusion has resolved. However, if the patient desires to continue on PD, a multitude of treatment options are available. These include conservative management with temporary interruption of PD, conventional pleurodesis, and surgical thoracotomy or video-assisted thoracoscopic (VATS) repair of the diaphragmatic defect. The underlying goal of treatment is simple: prevent recurrence of hydrothorax through the closure of the diaphragmatic defect. It is prudent to consult and discuss management plans with the thoracic surgical team. As no guidelines exist for the management of hydrothorax in PD patients, it is unclear which approach confers the best long-term outcomes.
Temporary Interruption of Peritoneal Dialysis (Conservative Management)
There is a clear consensus that interruption of PD should be the initial step in the definitive management of hydrothorax. It is believed that discontinuation of PD acts to reduce the size of the effusion and in some cases promote spontaneous resolution of the pleuroperitoneal communication. It is thought that the acidic hypertonic PD fluid may act as an irritant and hence a sclerosing agent to close small defects in the hemidiaphragm. Discontinuation of PD should occur for a period of 2 to 6 weeks. , A temporary transfer to HD often is necessary, especially if the patient has limited residual renal function. Using this approach, one case series noted a 53% success rate in the return to long-term PD. However, a high recurrence rate also was noted.
Occasionally, patients who experience hydrothorax on CAPD are able to resume PD by cycler after only being treated with conservative measures (i.e., temporary interruption of PD). As previously mentioned, the main determinants of IAP are volume and position, and therefore a dialysis prescription emphasizing low-volume, supine-based dialysis should be initiated in these patients. Although somewhat counterintuitive, the supine position is not conducive to fluid migration into the pleural cavity. One explanation is that the decrease in IAP afforded by the supine position more than compensates for the movement of fluid into the pleura when supine.
Pleurodesis is another option for repairing the pleuroperitoneal communication leading to hydrothorax. This method involves the instillation of a sclerosing agent into the pleural cavity, which causes an inflammatory reaction, leading to pleural fibrosis and subsequent obliteration of the diaphragmatic defect. No consensus has emerged regarding the optimal timing for pleurodesis. Some have proposed using it concurrently with conservative measures, whereas others have advocated its use as a second-line measure after conservative treatments have failed.
Several agents have been used successfully for pleurodesis. These include talc, tetracycline, autologous blood, fibrin glue, and hemolytic streptococcal preparation OK-432. Pleurodesis can be undertaken via the chest tube or now, more commonly as part of a VATS procedure. This enables direct visualization to ensure effective talc poudrage as well as identification of diaphragmatic defects. Tetracycline and talc appear to have similar success rates.
Some authors advocate for the resumption of PD as early as 10 days after pleurodesis. In contrast, others favor a more conservative strategy opting to resume PD after 4 to 6 weeks. Although it is currently unclear which is the best approach, the use of pleurodesis in the management of hydrothorax is associated with good long-term results. In fact, a large systematic review demonstrated 48% of patients treated with pleurodesis were able to resume long-term PD.
VATS has become the preferred modality to obliterate the diaphragmatic defect as the pleuroperitoneal communication can be directly visualized. The “blebs” in the diaphragm often can be seen and then sutured, stapled, or reinforced with Teflon patches. As previously described, VATS is also an effective vehicle for pleurodesis. It is recommended that 2 to 3 L of dialysate be infused intraoperatively at the conclusion of the procedure to ensure that there is no seepage of dialysate indicating an ongoing defect. Surgery utilizing a thoracotomy is significantly invasive and reserved as a last resort. Unsurprisingly, recurrence rate is highest when the communication is not detected at the time of surgery. VATS treatment of hydrothorax has been associated with excellent long-term outcomes. In one study, 88% of patients were able to resume long-term PD without recurrence of hydrothorax.
Malfunction of the Peritoneal Catheter
Malfunction of the peritoneal dialysis catheter is one of the most common complications of PD occurring in up to 20% of patients, not infrequently necessitating transfer to HD.
Malfunction frequently manifests early in the course of PD and is highlighted by poor drainage from the catheter.
Drainage problems can be broken down into “one-way obstruction,” which involves adequate inflow but poor outflow; and “two-way obstruction,” which entails both poor inflow and outflow.
The primary causes of catheter malfunction are summarized in Table 33.5 .
|One-way obstruction||Constipation—stool extrinsically impinges on catheter||Poor dialysate outflow |
Evidence of fecal loading on abdominal x-ray
|Laxatives, stool softeners, suppositories; omission of constipating agents such as iron, calcium, and opioids peri-insertion|
|Catheter tip migration (may be precipitated by constipation; intestinal peristalsis)||Poor dialysate outflow |
Catheter tip incorrectly positioned on abdominal x-ray
|Radiological manipulation |
Surgical manipulation or replacement, often laparoscopic
|Extraluminal occlusion by omentum, adhesions, or catheter “engulfment” by fallopian tube fimbriae||Poor dialysate outflow |
Abdominal x-ray may or may not show catheter displacement
|Forceful flushing—but risk for mechanical damage |
Surgical manipulation—omentopexy can be performed.
Laparoscopic “salpingopexy” or salpingectomy when obstructed by fallopian tube
|Two-way obstruction||Intraluminal catheter occlusion by thrombus/fibrin||Poor dialysate inflow and outflow |
Adhesions may be visible on CT peritoneography—limited distribution of dialysate is suggestive
|Heparin in dialysate: 500 units/L |
Urokinase: instilled for 1 h
|Catheter kinking||Poor dialysate inflow and outflow||Catheter manipulation—radiological vs. surgical |
At the time of insertion, the operator should check for good inflow and outflow
Poor catheter outflow is usually the result of obstruction around the holes in the intraperitoneal portion of the dialysis catheter. During instillation of dialysate, the increased pressure pushes away the obstruction, so inflow is preserved. However, with the negative Bernoulli force involved in drainage of effluent, the obstructing material comes into contact with the catheter and envelopes it, limiting outflow. A 2006 case series reported that catheter tip migration was the most common cause of one-way obstruction of the PD catheter. A more recent retrospective pediatric study reviewed 452 access revisions over an 8-year period. Sixty percent of the access revisions were for mechanical obstruction and this doubled the risk for technique failure compared with infectious causes.
Investigating for causes of poor outflow or one-way obstruction should begin with a plain abdominal x-ray. This is a simple technique that allows for easy identification of the common causes, namely, constipation and catheter migration. If the abdominal film does not identify a cause, then a CT can be undertaken with contrast injected through the PD catheter. A catheter dye study can suggest omental wrap or adhesions as causes of outflow obstruction ( Fig. 33.6 ).
An uncommon but nonetheless important cause of catheter malfunction is obstruction by fallopian tube fimbriae. Direct visualization by laparoscopy is thought to be the most efficient diagnostic tool for this complication not least because catheter manipulation along with salpingopexy or salpingectomy can be undertaken if appropriate.
The management of outflow obstruction is dependent on the cause. Constipation usually can be easily treated with judicious laxative use; this may be sufficient to restore catheter function. It is prudent to try this approach even in the absence of radiological evidence of constipation. It is important to ensure that other potentially constipating medications such as iron and calcium are held temporarily before catheter insertion as these medications may contribute to constipation.
For catheter tips that have migrated into the upper abdomen, a guidewire can be inserted through the PD catheter radiologically to enable maneuver back to the pelvis. Although successful repositioning will occur in almost all patients, the rate of recurrence is high with long-term patency being <50%. Laparoscopic manipulation or catheter replacement is frequently used and can be particularly appropriate for the management of omental wrap.
In recent years, tacking of the omentum to the upper abdomen, or omentopexy, has been performed at the time of laparoscopic PD catheter insertion in an attempt to prophylactically avoid future problems. A retrospective review of PD catheter insertions performed over a 10-year period showed that “advanced” laparoscopic insertion using the creation of a rectus sheath tunnel, selective omentopexy, and adhesiolysis significantly reduced catheter dysfunction rate and increased PD longevity.
Problems with both inflow and outflow, or two-way obstruction, are usually the result of intraluminal obstruction or a kink in the PD catheter. There have been multiple case reports highlighting materials that cause intraluminal obstruction. These include blood clots, cryoglobulins, fibrin strands ( Fig. 33.7 ), stones, and fungal balls. ,
Before initiating a diagnostic workup for suspected two-way obstruction flushing the catheter under high pressure with heparinized saline followed by aspiration should be attempted. If this maneuver is unsuccessful, then tissue plasminogen activator (tPA) should be instilled and allowed to dwell for a few hours to lyse old clots or other foreign material. , The transfer set should be inspected to ensure it is not occluded with fibrin.
If the catheter obstruction persists, then a diagnostic workup similar to that of one-way obstruction should be implemented. If an occlusion or kink in the PD catheter is found, a guidewire or balloon can be inserted via the catheter using a fiberscope. Alternatively, surgical manipulation via a laparoscopic approach can be undertaken and has yielded positive results.
Drain pain during PD is a commonly encountered problem. It frequently occurs during training and can negatively affect a patient’s progress as well as confidence levels. Despite this, there is a paucity of published data regarding the problem. A Canadian survey questioned 293 patients on automated PD and found that 72 were using a tidal modality. Of these, 25% had been started on tidal dialysis in an attempt to alleviate drain pain.
The precise cause of drain pain is unclear. However, it is usually a problem occurring during cycler usage. Postulated explanations have therefore included the application of negative pressure to the sensitive parietal peritoneum during the hydraulic suction of the cycler. Another theory relates to suction on the bowel wall. In addition, it has been suggested that low catheter insertion sites may be contributory as a result of the catheter tip being more likely to be in contact with parietal peritoneum.
Tidal PD was first introduced as a method to increase contact time of dialysis fluid with the peritoneal membrane and so improve solute clearance. In tidal PD, a residual volume is left in the peritoneal cavity. For example, for a patient with a 2 L dwell volume, 85% tidal flow would imply that after the first 2 L infusion, 1.7 L (rather than 2 L) is drained, and the next inflow and outflows are again 1.7 L until the final drain, when all the residual fluid is drained. Therefore during this process a residual volume resides in the peritoneal cavity. Due to its relative complexity, tidal PD is not used often for clearance purposes, but can be very helpful in those with inflow and outflow pain. The tidal volume can be increased even further (e.g., to 50%). In the past, there were some concerns regarding the use of tidal volumes as the rates of increased intraperitoneal volume events or “overfill” were increased. However, newer cyclers guard against this by continuing to suck on an empty peritoneal cavity that can then unfortunately lead to worsening drain pain. If this fails to alleviate symptoms, a switch to CAPD may be needed; drainage is gentler and less likely to incur symptoms.