Peritonitis in peritoneal dialysis: CT findings and role

Clinical History

An elderly male presented with hypertension, end-stage renal impairment with biopsy-confirmed tubular-interstitial atherosclerotic damage, on ambulatory peritoneal dialysis since 2 years, previous cholecystectomy, brain haemorrhage and resected colon adenoma.
Currently febrile (up to 38°C), with abdominal pain and turbid peritoneal effluent, lower limb oedema and worsening renal function.

Imaging Findings

At admission, plain abdominal radiographs (Fig.1) showed normally positioned peritoneal dialysis catheter, appearance of air-fluid levels in distended transverse colon and centralised small bowel loops.
Despite hospitalization, prompt antibiotic and diuretic therapy, the patient experienced uraemic symptoms including vomiting, profound malaise and mental confusion; laboratory tests revealed further increase of serum creatinine (13 mg/dl compared to 8.5 mg/dl a month earlier) and metabolic acidosis.
Unenhanced and post-contrast CT including panoramic coronal reconstructions (Figs.2,3) showed loculated peritoneal fluid in the perihepatic area and lesser sac, with mild uniform, non-calcified and enhancing serosal thickening, several bowel air-fluid levels. Tunnel infections and surgical causes of peritonitis were excluded. Effluent cultures diagnosed Enterococcus faecalis infection.
Despite transfer to haemodialysis, the patient could not recover from peritonitis.

Discussion

Peritoneal dialysis (PD) has become an established renal replacement therapy for one-third of newly diagnosed cases of end-stage renal disease, and may be performed either manually (continuous ambulatory PD) or using automated devices. Compared to haemodialysis, PD is preferred in patients with poor vascular access, diabetes or cardiovascular impairment, allows similar survival and better freedom. Unfortunately, long-term effectiveness is limited by inherent complications, mostly infectious rather than mechanical [1-4].
PD-associated peritonitis (PDAP) is by far the most prevalent complication (1 episode every 20-30 months per patient on average) and main cause of hospitalization and switch to haemodialysis, associated with significant mortality (3.5-10%). PDAP manifests with variable degrees of diffuse abdominal pain plus “cloudy” effluent, and accounts for 45.4% of acute abdomen cases in PD. According to international guidelines, PDAP is diagnosed on the basis of 2 out of 3 criteria namely (a) signs and symptoms; (b) leukocytosis >100 cells/mmc, >50% neutrophils in effluent, (c) one or more organisms cultured. Mostly caused by primary infection via dialysis catheter, PDAP should be promptly treated with antibiotics for at least 2 weeks. Catheter removal is required in refractory or relapsing PDAP, fungal and mycobacterial infections. Alternatively, 3.5 to 35% of PDAP cases are secondary to other intra-abdominal inflammatory conditions, particularly bowel ischemia or perforation (18.1%) and pancreatitis (13.6%), with mortality approaching 50% [1-5].
Traditionally, diagnostic imaging had limited role in PDAP. Albeit sometimes suggested by pronounced illness and sepsis, lactic acidosis, enteral material or multiple Gram-negative organisms in the dialysate, surgical peritonitis is often obscured by poor pain localisation and use of intraperitoneal antibiotics. Plain radiographs only allow identifying catheter position and free air, which is present in 27% of PDAP cases. Conversely, CT has additional value in detecting other causes of intra-abdominal sepsis and collections amenable to drainage. In PDAP, CT findings include: peritoneal thickening (45% of cases), loculated peritoneal fluid secondary to adhesions (38.1%, commonly associated with dialysis failure), and the rare but more specific serosal contrast enhancement (4.7%); conversely abscesses (7%) are uncommon due to altered peritoneal defense mechanisms against contamination [6-9].
Furthermore, mild enhancing peritoneal thickening may represent the earliest stage of encapsulating peritoneal sclerosis (EPS) which occurs in 0.7-1% of PD patients, with prevalence increasing up to 20% after 8 years on PD. EPS progresses to form marked fibrotic serosal thickening and calcific plaques, which eventually become widespread and ultimately encase the small bowel loops [6, 8-10].

Differential Diagnosis List

Final Diagnosis

Peritoneal dialysis-associated peritonitis.

URL:	https://eurorad.org/case/14334
DOI:	10.1594/EURORAD/CASE.14334
ISSN:	1563-4086