In this article, we described an unusual clinical course of a CAPD patient who suffered from peritoneal adhesion due to CAPD-related peritonitis. The complication was serious enough to compromise her CAPD, but was so specific that it prevents the invasion of a potentially lethal infection.
Peritonitis remains a leading complication of PD and contributes greatly to morbidity and mortality of PD patients [7]. Severe peritonitis can cause peritoneal membrane failure and stays as the major cause of discontinuing PD and shifting to HD. Peritonitis infected by Gram’s (−) bacteria has become more common, although Gram’s (+) organisms remain the major causes [3]. Previous study has shown that Pseudomonas aeruginosa peritonitis is generally severe and associated with longer duration of admission, more severe peritoneal membrane damage, and higher rate of catheter removal and transfer to HD [8]. Therefore, some even suggested prompt catheter removal upon diagnosis of Pseudomonas peritonitis for better outcomes [9]. Our patient, in her second peritonitis event, was successfully treated with antibiotics for one month and continued her PD treatment. However, PD inadequacy soon became evident and this was also proved by follow-up peritoneum equilibration test. Her Kt/V decreased from 1.99 to 1.44, and weekly creatinine clearance dropped from 56 liters per week to 41 liters per week. These findings and severe edema persuaded her to switch to HD.
We had cautiously considered the possible diagnosis of encapsulated peritoneal sclerosis (EPS), the most serious complication of long-term PD therapy, because the treatment of EPS was usually unsatisfactory and outcome could be poor with high mortality rate [10]. This patient presented several risk factors associated with EPS development, including long duration of PD, young age, exclusive use of dextrose solution, peritonitis, and late ultrafiltration failure. She also suffered from gradual reduction of appetite, progressive weight loss (obvious peripheral edema but unvarying body weight), malnutrition (serum albumin < 3.5 g/dl for almost a year before shifting to HD), and favorable structural finding noted during laparotomy. However, she did not experience symptoms and signs of bowel obstruction that are common in patients with severe EPS, such as progressive abdominal pain, abdominal distention, or difficulties in defecation. The poor appetite and peripheral edema were effectively corrected by changing treatment modality without specific treatment for EPS, such as enterolysis [11], tamoxifen [12], or immunosuppressive agents [13]. In the most severe form of EPS, a sclerotic layer may completely cover the intestines, which gives them the appearance of a cocoon. The CT images supported the diagnosis of EPS and cocoon formation, but they also showed that the adhesion and fibrosis were relatively mild in the peritoneum between intestines. This might partly explain the absence of excruciating abdominal symptoms of bowel obstruction.
This patient did not experience any traumatic event that might lead to her bowel perforation. The most reasonable explanation would still be the adhesion between the intestines and abdominal wall at the insertion site. She had kept her Tenckhoff catheter for about two months before removal. With hindsight, the catheter might have been pulled unintentionally, thus tearing and bowel wall. Nevertheless, the tear was too small to cause significant abdominal symptoms, as shown by the clinical wellness and improvement in the period before Tenckhoff catheter removal. The leakage still was manifested by large amount of intra-abdominal pus accumulating gradually between the parietal and visceral peritoneal membranes, within the same period of time. It’s very likely that the peritoneal cavity was completely covered by a fibrotic layer and the pus did not gain access into the intestinal loops. Therefore, this patient could live a life of wellness devoid of any significant gastrointestinal symptoms in those two months of HD. Pus was later drained smoothly with pigtail catheters and the bowel perforation was then successfully closed.
In summary, this patient had suffered from peritonitis-related peritoneal adhesion severe enough to cause ultrafiltration failure that made her change dialysis modality. Diagnosis of EPS was supported by image findings. Nevertheless, the pattern of adhesion was so specific that kept the pus out of her intestinal loops and salvaged her from the anticipated abdominal catastrophe.