To the Editor:
Intraperitoneal viscera inflammation favours the translocation of polymorphonuclear leukocytes to the peritoneal cavity, with some cases of cloudy peritoneal effluent being reported alongside infection of the colon by Clostridium difficile.1
We report the case of an 87-year-old male with a good quality of life, who had long-term high blood pressure, chronic obstructive pulmonary disease with bronchiectasis and stage 5 chronic kidney disease secondary to nephroangiosclerosis, with a baseline glomerular filtration rate of 15ml/min. He came to our hospital due to deterioration in his general condition, asthenia and anorexia, and his blood tests revealed a decrease in his glomerular filtration rate (7ml/min). There was no change in his normal medication or focal infection. In the following days, he did not respond to conservative measures and, with the patient’s consent, we started renal replacement therapy by peritoneal dialysis, with a double-cuff straight Tenckhoff peritoneal catheter being introduced, without complications during the procedure. In the hours following the procedure, the patient presented with fever and increasing coughing and expectoration. The X-ray was suggestive of right lower pulmonary lobe consolidation, and as such, given the suspicion of nosocomial pneumonia, we started treatment with meropenem and ciprofloxacin. He started automatic peritoneal dialysis (APD) a week later, given the progressive deterioration of kidney function. He was discharged ten days later having recovered his baseline clinical condition, with oral antibiotic treatment and the indication of continuing APD in the peritoneal dialysis unit while awaiting training. The microorganism was not isolated in the blood cultures or in the sputum analysis.
Four days later, after the weekend period, he came to the hospital complaining of watery diarrhoea, without pathological products, lasting 24 hours. He had abdominal discomfort and fever and cloudy peritoneal effluent was observed. The fluid analysis revealed 408 cells/ul with a predominance of polymorphonuclear cells (79%). Using clinical and cytological criteria, the patient was diagnosed with peritonitis and empirical treatment was started with intraperitoneal ceftazidime and vancomycin.2 Given the lack of response to treatment or growth of the microorganism in the peritoneal dialysate culture, after three days we received the stool culture result, which revealed the presence of Clostridium difficile toxin and antigen.
Given the absence of clinical improvement and the persistence of cloudy dialysate, the case was reassessed and we considered other causes of cloudy peritoneal effluent with polymorphonuclear predominance.3 We unsuccessfully searched for fungi and mycobacteria. The patient had not received treatment with vancomycin or amphotericin B before symptoms started. The results of the studies to determine the presence of Clostridium difficile toxins or antigens in peritoneal dialysate were negative. Other symptoms that may include the presence of sterile cloudy liquid with eosinophil predominance3 were not suggestive in this patient, based on the chronology with regard to catheter insertion. The X-ray of the abdomen did not display pneumoperitoneum. The existence of an inflammatory intestinal process and the negative results of tests carried out led us to consider the presence of sterile cloudy peritoneal dialysate to be secondary to colitis due to Clostridium difficile. We discontinued intraperitoneal antibiotic administration and started the patient on 500mg of metronidazole administered orally every 8 hours, with little response. As such, we decided to combine it with 500mg of vancomycin administered orally every 8 hours, with the patient displaying a gradual improvement of the process, a decrease in the frequency of bowel movements and an increase in density of stools. The transparency of the peritoneal dialysate was simultaneously recovered.
The fact that no Clostridium difficile toxins or antigens were detected in the peritoneal dialysate suggests that the aetiology of the cloudy dialysate corresponds to the passage of leukocytes and not to phenomena of bacterial translocation with secondary peritonitis. The fact that symptoms only improved with the introduction of oral vancomycin in the treatment supports this hypothesis. There are studies that report that the exposure of intestinal epithelial cells to the toxin Clostridium difficile modulates the epithelial expression of IL-8 and the intercellular adhesion molecule 1 (ICAM-1), involved in the chemoattraction and adhesion of leukocytes.4 Furthermore, the data suggest that the transmigration of leukocytes to the peritoneal cavity is related to the upward regulation of ICAM-1 receptors.5 These results together may offer an explanation of the pathophysiology of the symptoms described.
Conflicts of interest
The authors declare that they have no conflicts of interest related to the contents of this article.
