PERSISTENT SYMPTOMATIC INTRA-ABDOMINAL COLLECTION AFTER CATHETER REMOVAL FOR PD-RELATED PERITONITIS

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1 Peritoneal Dialysis International, Vol. 31, pp doi: /pdi /11 $ Copyright 2011 International Society for Peritoneal Dialysis PERSISTENT SYMPTOMATIC INTRA-ABDOMINAL COLLECTION AFTER CATHETER REMOVAL FOR PD-RELATED PERITONITIS Cheuk-Chun Szeto, Bonnie Ching-Ha Kwan, Kai-Ming Chow, Wing-Fai Pang, Vickie Wai-Ki Kwong, Chi-Bon Leung, and Philip Kam-Tao Li Department of Medicine & Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, China Background: Peritoneal dialysis (PD) patients with severe peritonitis require catheter removal. It is often assumed that this approach, together with antibiotics, would eradicate the infection; however, some patients continue to have problems despite catheter removal. Method: We reviewed 30 consecutive PD patients in our center from 1997 to 2008 with recurrent loculated peritoneal collection after catheter removal for severe peritonitis. Results: Of the 1928 episodes of peritonitis that occurred in 702 patients during the study period, 11.1% required catheter removal and 1.6% developed recurrent peritoneal collection that required percutaneous drainage. Median time to diagnosis of intra-abdominal collection was 12 days after catheter removal (interquartile range 7 61 days). In 25 patients (83.3%), aspirate of the abdominal collection was culture negative. In 17 patients (56.7%), the abdominal collection was recurrent and required repeated percutaneous aspiration. Only 3 patients had successful reinsertion of the peritoneal catheter but all had reduced small solute clearance after returning to PD. Conclusion: A small but not negligible proportion of patients with PD-related peritonitis develop recurrent intraabdominal collection that requires percutaneous drainage after catheter removal. The chance of a successful return to PD is very low in this group of patients. Direct conversion to long-term hemodialysis may avoid unnecessary attempts at peritoneal catheter reinsertion. Perit Dial Int 2011; 31:34-38 epub ahead of print: 6 May doi: /pdi KEY WORDS: Renal failure; infection; ascites. Peritonitis is a serious complication of peritoneal dialysis (PD) and probably the most common cause of Correspondence to: C.C. Szeto, Department of Medicine & Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, China. ccszeto@cuhk.edu.hk Received 10 September 2009; accepted 29 March technique failure in PD (1 3). Although less than 4% of peritonitis episodes result in death (4), peritonitis is a contributing factor to death in 16% of deaths on PD (5). In Hong Kong, peritonitis is the direct cause of death in over 16% of PD patients (6). Refractory peritonitis, defined as failure to respond to appropriate antibiotics within 5 days, should be managed by removal of the catheter to protect the peritoneal membrane for future use (3,7,8). This approach is also recommended by the latest guideline for the management of PD-related infections, published by the International Society for Peritoneal Dialysis (ISPD) in 2005 (9). In general, effective systemic antibiotics should be continued for another 1 2 weeks after catheter removal. Although peritoneal adhesions may prevent reinsertion of the catheter, or continuation on PD may not be possible due to permanent membrane failure (3,9), most patients should, in theory, be adequately treated and the infection eradicated using this approach. Accumulating evidence suggests, however, that a small proportion of patients continue to have problems. For example, Bilgic et al. (10) found that 8 of their 26 patients that were transferred from PD to hemodialysis had loculated intra-abdominal fluid collection. In another study, Moon et al. (11) found that 22.2% of patients with peritonitis-related technique failure had recurrent ascites; the risk was particularly high for those patients with persistently elevated serum C-reactive protein levels, indicating the possibility of ongoing infection. Here we review 30 consecutive PD patients with recurrent peritoneal collection after catheter removal for severe peritonitis. PATIENTS AND METHODS PATIENT SELECTION All PD patients at our center gave written consent for reviewing their clinical data when they entered the di- 34

2 PDI JANUARY 2011 VOL. 31, NO. 1 ABDOMINAL COLLECTION AFTER PERITONITIS alysis program. All episodes of PD peritonitis in our unit from 1997 to 2008 were reviewed. Data were collected by reviewing the Hong Kong Renal Registry database as well as the hospital records of individual patients by the investigators. The diagnosis of peritonitis was based on at least two of the following (12,13): (1) abdominal pain or cloudy peritoneal dialysis effluent (PDE); (2) leukocytosis in PDE (>100/mL); and (3) positive Gram stain or culture of PDE. Episodes with peritoneal eosinophilia but negative bacterial culture were excluded. During the 12-year study period, we identified 30 patients (14.0%) from whom the catheter had been removed and that had subsequent loculated intraabdominal collection requiring percutaneous drainage. Their clinical records were reviewed. In essence, the baseline and clinical data, including age, sex, underlying renal disease, PD regimen, and history of peritonitis, were recorded. Comorbid conditions were also recorded. The modified Charlson Comorbidity Index, which has been validated in PD patients (14), was used to calculate a comorbidity score. The results of peritoneal equilibration tests were also reviewed. PATIENT MANAGEMENT Peritonitis episodes were treated with the standard antibiotic protocol of our center, which has changed systemically over time (15). Initial antibiotics for peritonitis were generally intraperitoneal administration of a third- or fourth-generation cephalosporin, plus or minus vancomycin, or cefazolin plus gentamicin. Antibiotic regimens for individual patients were modified when PDE culture results became available. We followed standard guidelines for antibiotic dosages (9,13). In general, patients received antibiotics for at least 14 days. For peritonitis episodes caused by Staphylococcus aureus, Pseudomonas, or Stenotrophomonas species, treatment with two effective antibiotics was given for at least 21 days. In general, S. aureus peritonitis was treated with cefazolin or vancomycin; most patients also had rifampicin as the adjunct therapy. Pseudomonas peritonitis was generally treated with an aminoglycoside and a thirdgeneration cephalosporin. As described in our previous report (3), if the PDE did not clear up by day 5 10 despite in vitro sensitivity of the bacterium, the Tenckhoff catheter was removed without peritoneal lavage. Nevertheless, the actual timing of Tenckhoff catheter removal varied for individual patients due to the availability of an operating theater. In general, we did not perform an abdominal CT scan before catheter removal. After catheter removal, patients were put on temporary hemodialysis and the appropri- ate antibiotic therapy was continued for another 2 weeks. In asymptomatic patients, we did not screen for recurrent intra-abdominal collection after catheter removal. Imaging study (either ultrasound or CT scan) was arranged only for patients with persistent abdominal symptom or features of ongoing infection. In patients in whom intra-abdominal collection was identified, percutaneous diagnostic and therapeutic drainage by simple aspiration or pigtail catheter drainage was performed under radiological guidance. In general, needle aspiration was used. Pigtail drainage was left in situ for loculated effusion or recurrent collections. As described previously (3), patients were switched to long-term hemodialysis only when attempts of Tenckhoff catheter reinsertion failed because of peritoneal adhesion, or when there was ultrafiltration failure due to peritoneal sclerosis. Tenckhoff catheter reinsertion was attempted at least 4 weeks after the old Tenckhoff catheter was removed. STATISTICAL ANALYSIS Statistical analysis was performed using SPSS software version 15.0 (SPSS Inc., Chicago, IL, USA). All data are expressed as mean ± SD or median [interquartile range (IQR)]. RESULTS From 1997 to 2008, 1928 episodes of PD-related peritonitis were recorded in 702 patients of our unit. The overall peritonitis rate was 1 episode/24.2 patient-months of follow-up. In 214 episodes (11.1%), catheter removal was required. We analyzed 30 patients (14.0%) that had loculated intra-abdominal collection requiring percutaneous drainage after catheter removal due to refractory peritonitis. The baseline clinical characteristics are summarized in Table 1. The median number of previous peritonitis episodes was 2 (IQR 0 4); in 9 patients, the index episode represented the first episode of peritonitis. The microbiological causes of the peritonitis episodes are summarized in Table 2. In short, nearly half the episodes were caused by Pseudomonas species. Twenty patients (66.7%) were initially treated with cefazolin plus ceftazidime; the initial treatment for the rest was cefazolin plus netilmicin (7 patients) or vancomycin plus ceftazidime (3 patients). CLINICAL FEATURES Median time from onset of peritonitis to catheter removal was 9 days (IQR 6 13 days). We did not find any 35

3 SZETO et al. JANUARY 2011 VOL. 31, NO. 1 PDI TABLE 1 Baseline Characteristics of the Patients Patients (n) 30 Sex (M:F) 13:17 Age 48.3±12.3 years Duration of dialysis a 63.7 ( ) months Body height 160.6±9.8 cm Body weight 57.4±9.1 kg Diagnosis [n (%)] Glomerulonephritis 11 (36.7) Diabetes 5 (16.7) Polycystic 4 (13.3) Obstruction 2 (6.7) Others/unknown 8 (26.7) Major comorbidity [n (%)] Coronary heart disease 4 (13.3) Cerebrovascular disease 2 (6.7) Diabetes 7 (23.3) Charlson index score 4.0±1.6 Previous peritonitis a 2 (0 8) episodes a Median (range). TABLE 2 Microbiological Cause of the Peritonitis Organisms identified Staphylococcus aureus 3 a Pseudomonas species 14 Escherichia coli 3 Other gram-negative bacilli 2 Fungi 1 Polymicrobial 1 Culture negative 6 b Total 30 a 2 episodes were methicillin-resistant S. aureus. b 2 patients had peritonitis within the preceding 4 months (E. coli, 1 case; culture negative, 1 case). clinical parameters that could predict the development of intra-abdominal collection. For example, there was no difference in the initial presentation or baseline PDE leukocyte count between patients that subsequently developed intra-abdominal collection and those that required catheter removal but did not have a collection, nor was there a significant difference in PDE leukocyte count on day 3 or 5, or percentage of PDE leukocyte reduction on those days (details not shown). Presenting symptoms included persistent fever (17 patients), persistent abdominal pain (12 patients), clinical bowel obstruction (21 patients), persistent leukocytosis (20 patients), elevated inflammatory markers N (20 patients), and clinical ascites (7 patients). Median time of diagnosis of intra-abdominal collection was 12 days after catheter removal (IQR 7 61 days). In 24 patients, contrast CT scan of the abdomen was performed. The findings are summarized in Table 3. MANAGEMENT AND OUTCOME All patients underwent percutaneous drainage under ultrasound guidance. In 25 patients (83.3%), aspirate of the abdominal collection was culture negative and differential cell count revealed a predominance of macrophages in the drainage fluid. The same organism was isolated from abdominal aspirate in 3 patients, while the organism from abdominal aspirate was different from that of the PDE in 2 patients. In 17 patients (56.7%), the abdominal collection was recurrent and required repeated percutaneous aspiration. For those patients that required more than one percutaneous aspiration, the median number of aspirations was 3 (IQR 2 4). None of the patients was treated with systemic steroid or tamoxifen for a sterile abdominal aspirate. Of the 30 patients, 9 died before any attempt of Tenckhoff catheter reinsertion was possible. The causes of death were persistent peritonitis with or without overt septicemia (7 patients) and myocardial infarction (2 patients). Two patients had post-mortem examination; both showed nonspecific peritoneal inflammation without overt peritoneal sclerosis. Median survival of the other 21 patients was 41.9 (range ) months; 4 patients died within 12 months (2 due to chest infection, 1 due to myocardial infarction, 1 in whom dialysis was terminated due to poor quality of life). Two patients had subsequent hospital admissions for bowel obstruction; neither patient had overt encapsulating peritoneal sclerosis (EPS) and both responded to conservative management. Other than the 9 patients that died within 6 weeks of catheter removal, reinsertion of a Tenckhoff catheter was TABLE 3 Summary of Contrast Abdominal CT Scan Finding Patients (n) Total 24 Peritoneal enhancement 3 Peritoneal thickening 11 Peritoneal calcification 1 Small or large bowel thickening 3 Adhesions of bowel loops 14 Signs of bowel obstruction 4 Fluid loculation or septation 24 36

4 PDI JANUARY 2011 VOL. 31, NO. 1 ABDOMINAL COLLECTION AFTER PERITONITIS attempted in the other 21 patients, but only 3 could resume PD. Catheter reinsertion failed in the other 18 patients because of peritoneal adhesion (15 patients) or limited intra-peritoneal space (3 patients). None of the 18 patients developed overt EPS during follow-up. All 3 patients that had catheter reinsertion, however, had reduced small solute clearance after returning to PD (Table 4). DISCUSSION In the present study, we found that 1.6% of patients with PD-related peritonitis developed recurrent intraabdominal collection that required percutaneous drainage after removal of the Tenckhoff catheter. The incidence of recurrent intra-abdominal collection after peritonitis in the present study appears to be lower than in previous reports (10,11). A number of possible explanations could account for the discrepancy. Notably, previous series included asymptomatic patients with ascites fluid found incidentally (10) and patients that were converted to long-term dialysis and developed delayed ascites, which could be related to hemodialysis rather than the original episode of peritonitis (11). In addition, our patients were more aggressively treated with antibiotics before catheter removal and a double antibiotic regimen was often given (16,17), which may account for the lower incidence of subsequent fluid collection. In general, we performed percutaneous drainage of the collection; repeated aspiration was sometimes needed because of recurrent or multi-loculated collection. Theoretically, our patients may represent either collection with an infective origin or loculated ascites secondary to intra-abdominal adhesions. In clinical practice, however, it is often difficult to discern the two. In this series, 16 patients were still receiving antibiotics when peritoneal collection was diagnosed and antibiotics were changed only if there was a positive Gram stain or clinical evidence of ongoing infection. Because 40% of the patients required repeated aspiration, therapeutic strategies to prevent recurrent collection (and probably to preserve the peritoneal membrane) would be an interesting area for further research. For example, intrapleural fibrinolytic therapy confers significant benefit in reducing the requirement for surgical intervention in patients with complicated parapneumonic effusion or overt empyema (18). It remains to be seen if a similar approach would work for abdominal collection after peritonitis. There are a few inadequacies in the present study. In this series, we did not study patients with EPS. In fact, we reviewed only the patients with intra-abdominal collection that required percutaneous drainage. It is our clinical impression that many asymptomatic patients would have ascitic fluid found during an attempt to reinsert a Tenckhoff catheter. Because we did not screen for abdominal collection after Tenckhoff catheter removal in all patients, the exact number of patients with this problem is unknown and our series likely represents the tip of the iceberg. On the other hand, the clinical significance of asymptomatic abdominal collection is poorly defined. Since a substantial proportion of our patients had intra-abdominal collection and clinical bowel obstruction, it is possible that some of the patients actually had an early form of EPS. However, findings on abdominal CT were substantially different between our patients (see Table 3) and published series of EPS (19), and few patients had recurrent intestinal obstruction, suggesting that most of our patients did not have EPS. It is also important to realize that the baseline peritoneal transport presented in Table 4 represents the value at the initiation of PD. In theory, it would be ideal to know the peritoneal transport characteristic shortly before the onset of peritonitis. Unfortunately, our unit did not have a policy of regular peritoneal equilibration testing for all PD patients. It could be argued that, in many of our patients, the Tenckhoff catheter was not removed promptly despite poor response to antibiotics. Median time from onset of TABLE 4 Summary of Peritoneal Transport Characteristics At initiation of PD Previous After return to PD Patient Sex/Age D/P4 MTAC Duration of dialysis peritonitis (n) Organism D/P4 MTAC 1 F/ months 1 Klebsiellas sp M/ months 0 Pseudomonas sp F/ months 2 Pseudomonas sp PD = peritoneal dialysis; D/P4 = dialysate-to-plasma creatinine ratio at 4 hours; MTAC = mass transfer area coefficient of creatinine (in ml/min/1.73 m 2 ). 37

5 SZETO et al. JANUARY 2011 VOL. 31, NO. 1 PDI peritonitis to catheter removal was 9 days in this series, which is substantially longer than the current recommendation (9). As described in our previous studies (16,17), catheter removal was not infrequently delayed in our center because of practical difficulties. It remains unknown to what extent delayed catheter removal contributed to the development of recurrent abdominal collection, and whether performing peritoneal lavage during catheter removal would prevent the development of a collection. In summary, we report a series of 30 patients with recurrent abdominal collection after catheter removal for PD-related peritonitis. The chance of successful return to PD is very low in this group of patients. Direct conversion to long-term hemodialysis may avoid the unnecessary attempts of peritoneal catheter reinsertion. DISCLOSURES All authors declare no conflict of interest. ACKNOWLEDGMENT This study was supported in part by the CUHK research accounts and , and the Richard Yu Peritoneal Dialysis Research Fund. REFERENCES 1. Piraino B. Peritonitis as a complication of peritoneal dialysis. J Am Soc Nephrol 1998; 9: Oreopoulos DG, Tzamaloukas AH. Peritoneal dialysis in the next millennium. Adv Ren Replace Ther 2000; 7: Szeto CC, Chow KM, Wong TY, Leung CB, Wang AY, Lui SF, et al. Feasibility of resuming peritoneal dialysis after severe peritonitis and Tenckhoff catheter removal. J Am Soc Nephrol 2002; 13: Mujais S. Microbiology and outcomes of peritonitis in North America. Kidney Int Suppl 2006; (103):S Fried LF, Bernardini J, Johnston JR, Piraino B. Peritonitis influences mortality in peritoneal dialysis patients. J Am Soc Nephrol 1996; 7: Szeto CC, Wong TY, Chow KM, Leung CB, Li PK. Are peritoneal dialysis patients with and without residual renal function equivalent for survival study? Insight from a retrospective review of the cause of death. Nephrol Dial Transplant 2003; 18: Choi P, Nemati E, Banerjee A, Preston E, Levy J, Brown E. Peritoneal dialysis catheter removal for acute peritonitis: a retrospective analysis of factors associated with catheter removal and prolonged postoperative hospitalization. Am J Kidney Dis 2004; 43: Krishnan M, Thodis E, Ikonomopoulos D, Vidgen E, Chu M, Bargman JM, et al. Predictors of outcome following bacterial peritonitis in peritoneal dialysis. Perit Dial Int 2002; 22: Piraino B, Bailie GR, Bernardini J, Boeschoten E, Gupta A, Holmes C, et al.; ISPD Ad Hoc Advisory Committee. Peritoneal dialysis-related infections recommendations: 2005 update. Perit Dial Int 2005; 25: Bilgic A, Sezer S, Ozdemir FN, Akgul A, Arat Z, Haberal M. Clinical outcome after transfer from peritoneal dialysis to hemodialysis. Adv Perit Dial 2006; 22: Moon SJ, Han SH, Kim DK, Lee JE, Kim BS, Kang SW, et al. Risk factors for adverse outcomes after peritonitis-related technique failure. Perit Dial Int 2008; 28: Vas SI. Peritonitis during CAPD. A mixed bag. Perit Dial Bull 1981; 1: Keane WF, Alexander SR, Bailie GR, Boeschoten E, Gokal R, Golper TA, et al. Peritoneal dialysis-related peritonitis treatment recommendations: 1996 update. Perit Dial Int 1996; 16: Beddhu S, Zeidel ML, Saul M, Seddon P, Samore MH, Stoddard GJ, et al. The effects of comorbid conditions on the outcomes of patients undergoing peritoneal dialysis. Am J Med 2002; 112: Szeto CC, Kwan BC, Chow KM, Law MC, Pang WF, Chung KY, et al. Recurrent and relapsing peritonitis: causative organisms and response to treatment. Am J Kidney Dis 2009; 54: Szeto CC, Chow KM, Leung CB, Wong TY, Wu AK, Wang AY, et al. The clinical course of pseudomonas peritonitis complicating peritoneal dialysis a review of 104 cases. Kidney Int 2001; 59: Szeto CC, Chow VC, Chow KM, Lai RW, Chung KY, Leung CB, et al. Enterobacteriaceae peritonitis complicating peritoneal dialysis: a review of 210 consecutive cases. Kidney Int 2006; 69: Cameron R, Davies HR. Intra-pleural fibrinolytic therapy versus conservative management in the treatment of adult parapneumonic effusions and empyema. Cochrane Database Syst Rev 2008; 2:CD Vlijm A, Stoker J, Bipat S, Spijkerboer AM, Phoa SS, Maes R, et al. Computed tomographic findings characteristic for encapsulating peritoneal sclerosis: a case-control study. Perit Dial Int 2009; 29: