peritoneal dialysis ( pd ) is a well - established means of renal replacement therapy .
a tenckhoff catheter is electively inserted into the peritoneal cavity before pd starts . after a healing period of at least two weeks
500  ml volumes are used for the first two days of training and titrated upwards , based on body surface area , over a two - week period .   in our centre , there are 3540 patients on pd at any one time .
approximately 2 patients join our program per month , and a similar number exit the program due to transplantation , switch to haemodialysis , or death .
patients starting pd in our unit use standard dextrose - based , lactate - buffered dialysate .
if infusion pain is a problem , bicarbonate / lactate buffered dialysate is used instead .
a daytime icodextrin - based dialysate dwell is often required in patients with little residual renal function for extra ultrafiltration .
the main complications of pd are either infectious , such as peritonitis and exit site infections , or pressure related , such as abdominal wall hernias and gastrooesophageal reflux .
this phenomenon appears to be due to increased intraabdominal pressure in the setting of congenital or acquired diaphragmatic defects .   the incidence rate of pleuroperitoneal leak development is thought to be less than 2% in newcomers to peritoneal dialysis .
we report three cases of pleuroperitoneal leak that occurred within a nine - month period at our institution .
this corresponded to a 12% incidence rate amongst newcomers to pd in that calendar year ( 25 newcomers ) . prior to that , there had been no cases in our department for over 10 years .
a 35-year - old philipino female presented to our unit with advanced chronic kidney disease , secondary to medullary cystic kidney disease , which was diagnosed many years earlier in the philipines .
one year later , she was approaching end - stage kidney disease and a tenckhoff catheter was inserted .
training for pd began four weeks later , using standard dextrose - based solutions .  
the high - pleural - fluid - serum - glucose ratio confirmed the clinical suspicion of a pleuroperitoneal leak .  
the pleural effusion resolved over a number of days with conservative management and the maintenance of a dry peritoneal cavity .
she had received two courses of heavy immunosuppression for this and was then lost to follow up . she had no known heart disease .
her renal ultrasound showed small , shrunken kidneys , which confirmed the suspicion of advanced chronic kidney disease .
acute hd was initiated but , as the patient 's preference was for pd , a tenckhoff catheter was inserted .
her target pd prescription consisted of four cycles of two litre exchanges with standard dextrose - based standard solution .
after six days of pd training , she presented with dyspnoea that was exacerbated by infusing dialysate .
she was seven kg above her dry weight and had clinical evidence of a rightsided pleural effusion and pedal oedema .
her electrocardiogram ( ecg ) and routine blood tests were unchanged . as she appeared volume overloaded , she had three litres of isolated ultrafiltration , using her central venous catheter .
again , she had 3 litres of isolated ultrafiltration . with this , she developed bad cramping .
although the initial presumed diagnosis was volume overload , the high pleural fluid glucose relative to the serum glucose confirmed the presence of a pleuroperitoneal leak ( table 2 ) . in accordance with patient preference , pd was discontinued and the tenckhoff catheter was removed .
a twenty - four - year - old irish male with a background history of congenital deafness , intellectual impairment and repair of a posterior urethral valve initially presented to the paediatric nephrology services with nephrotic syndrome . a renal biopsy revealed secondary focal segmental glomerulosclerosis and significant tubuleinterstitial fibrosis . following introduction of renin - angiotensin - aldosterone system blockade ,
a bicarbonate / lactate buffered solution was used to avoid infusion pain , which he would be unable to verbalise .
the following months were complicated by dialysis - associated pericarditis that resolved with intensive haemodialysis for a number of weeks .
his baseline pd prescription consisted of seven cycles of two litre exchanges with 1.36% dextrose solution .
five months later , he was admitted with clinical and radiological evidence of a large , rightsided pleural effusion with pleural thickening .
the exact duration of the effusion was unclear as he was unable to verbalise symptoms .
it was thought to have developed over weeks given the apparent absence of symptoms and the degree of pleural thickening .
the pleural fluid biochemistry was atypical for that seen with pleuroperitoneal leak ( table 3 ) .
however , as the patient was so well clinically , and numerous pleural fluid cultures were sterile , it was felt that the effusion was not related to infection .
it was also felt that the effusion was not due to volume overload given the degree of loculation within the effusion and the absence of other clinical signs of volume overload .
the low pleural fluid glucose and high lactate dehydrogenase ( ldh ) were difficult to interpret as the sampled fluid was walled off within a loculation , probably for many weeks .
the effusion did not resolve with drainage of the peritoneal cavity , and a chest drain was inserted .
this drain became dislodged and was replaced by a third drain with further intrapleural alteplase administration . at this point , however , a chest radiograph confirmed persistence of the large , loculated effusion with a small pneumothorax and a thick pleural rind .  
video - assisted thorascopic surgery with decortication was performed . a rapid postoperative recovery ensued and the postoperative chest drains were removed without event .
a chest radiograph six weeks later showed a well - expanded right lung , without effusion or pleural abnormality .
the first description of a pleuroperitoneal leak causing a pleural effusion in a pd patient was in 1967 . since then
, several reports have estimated the incidence of this complication ; the largest report estimated an incidence of 1.6% .  
it is thought that congenital or acquired communications between the pleura and peritoneum underpin this problem .
this had been demonstrated both in scintigraphy   and in autopsy specimens with localized absence of diaphragmatic muscle fibres .
the raised intraabdominal pressure with dialysate infusion , in a patient with such a communication , promotes the translocation of dialysate into the pleural space .  
this is probably related to the increased intraabdominal pressure in these patients and , therefore , higher pleuroperitoneal pressure gradients .
there is also a generalized connective tissue weakness in this condition that may contribute to inherent diaphragmatic weakness .
the timing of this complication varies from days to years after the initiation of pd .
half of cases occur within one month of starting pd ; these probably represent patients with congenital diaphragmatic defects .
presumably the preponderance of rightsided cases is due to diaphragmatic protection by the heart on the left .  
transudative effusions develop when systemic factors affect the pleural starling forces , as seen , for example , in congestive cardiac failure .
exudative effusions develop when local factors influence the formation of pleural fluid , as seen in malignant effusions .
light 's criteria are applied to the pleural and serum biochemistry to make the distinction between a transudate and an exudate .
an effusion is an exudate if the pleural - fluid - to - serum - protein ratio is > 0.5 or the pleural - fluid - to - serum - ldh ratio is > 0.6 .
transudative pleural effusions due to volume overload or congestive cardiac failure are relatively common in this population . in pd patients , such effusions
would typically be managed by increasing the dialysate volume and tonicity to increase ultrafiltration . however
, this can exacerbate the problem if the effusion is due to a pleuroperitoneal leak .
this highlights the importance of the pleural fluid glucose measurement . in the absence of loculation ,
a high pleural fluid to serum glucose concentration gradient is a very sensitive and specific test for diagnosing a pleuroperitoneal leak .
the ratio of pleural fluid to serum glucose is dynamic , and varies depending on the type of fluid instilled , the volume and the contact time .
this is due to the presence of hypertonic , usually dextrose - based , dialysate in the pleural space 
atypical biochemistry can be seen when the fluid has been in the pleural cavity for a prolonged period and has been partially reabsorbed by lymphatics , as seen in case 3 . other diagnostic tests are less practical and include technetium-99 m labelled peritoneal scintigraphy   and computed tomography ( ct ) with intraperitoneal dye . in terms of management ,
however , most cases of pleuroperitoneal leak are initially managed by drainage of the peritoneal cavity .
many patients choose to remain on hd in the long term and , therefore , formal repair of the diaphragm is not required . for those that wish to return to pd , there are a number of management options .
, thorascopic diaphragmatic repair was performed using absorbable polyglycolic acid felt , and fibrin glue .  
this allows resolution of the effusion and , in some cases , healing of the diaphragmatic defects .
a trial of low - volume pd two  six weeks later is successful in a significant proportion of cases .  
recurrent hydrothorax necessitates either a permanent switch to haemodialysis or definitive management of the pleural - peritoneal communication .
this method had relatively high rates of success , with 48% of patients resuming long - term pd after pleurodesis in one large systematic review .   
video - assisted thorascopic surgery , with direct visualization of the diaphragmatic defect and suture repair , has shown much promise in recent times for the management of this condition [ 13 , 14 ] . using this approach ,
88% of patients in one study successfully resumed long - term pd without recurrence .  
the three cases described above highlight the variability of this condition in terms of timing , symptoms , and management .
pleuroperitoneal leak should be considered in the differential diagnosis of a pleural effusion , particularly a rightsided effusion , in a patient on peritoneal dialysis .
 
 pressure related complications such as abdominal wall hernias occur with relative frequency in patients on peritoneal dialysis . 
 less frequently , a transudative pleural effusion containing dialysate can develop . 
 this phenomenon appears to be due to increased intra - abdominal pressure in the setting of congenital or acquired diaphragmatic defects .   
 we report three cases of pleuroperitoneal leak that occurred within a nine - month period at our institution . 
 we review the literature on this topic , and discuss management options . 
 the pleural effusion resolved in one patient following drainage of the peritoneum and a switch to haemodialysis . 
 one patient required emergency thoracocentesis . 
 the third patient developed a complex effusion requiring surgical intervention . 
 the three cases highlight the variability of this condition in terms of timing , symptoms and management . 
 the diagnosis of a pleuroperitoneal leak is an important one as it is managed very differently to most transudative pleural effusions seen in this patient population . 
 surgical repair may be necessary in those patients who wish to resume peritoneal dialysis , or in those patients with complex effusions . 
 pleuroperitoneal leak should be considered in the differential diagnosis of a pleural effusion , particularly a right - sided effusion , in a patient on peritoneal dialysis .  
 
1. Introduction
2. Case 1
3. Case 2
4. Case 3
5. Discussion