Ultrasound changes in sclerosing peritonitis following continuous ambulatory peritoneal dialysis

Ultrasound changes in sclerosing peritonitis following continuous ambulatory peritoneal dialysis

Clinical Radiology (1991)43, 176-179 Ultrasound Changes in Sclerosing Peritonitis Following Continuous Ambulatory Peritoneal Dialysis A. S. H O L L M...

2MB Sizes 0 Downloads 30 Views

Clinical Radiology (1991)43, 176-179

Ultrasound Changes in Sclerosing Peritonitis Following Continuous Ambulatory Peritoneal Dialysis A. S. H O L L M A N , M. A. M c M I L L A N * , J. D. BRIGGS*, B. J. R. J U N O R * and P. M O R L E Y Departments o f Radiology and * Renal Medicine, Western Infirmary, Glasgow

Sclerosis of the peritoneum, with encapsulation of the small bowel is one of the most serious complications of continuous ambulatory peritoneal dialysis (CAPD), and carries a high mortality. The abnormalities seen on ultrasound are described for 14 patients and comprise increased small bowel peristalsis, tethering of the bowel to the posterior abdominal wall, intraperitoneal echogenic strands and, in the late stages of the disease, membrane formation. Optimal visualization of these features in the early stages of the disease was obtained by examining the patients with dialysis fluid present in the abdomen. Sclerosing peritonitis should be suspected in patients being treated by CAPD who develop abdominal pain and progressive loss of ultrafiltration and subsequent investigation should include the use of ultrasound. Hollman, A.S., McMillan, M.A., Briggs, J.D., Junor, B.J.R. & Morley P. (1991). Clinical Radiology 43, 176-179. Ultrasound Changes in Sclerosing Peritonitis Following Continuous Ambulatory Peritoneal Dialysis Sclerosing peritonitis is recognized as a serious complication of both continuous ambulatory peritoneal dialysis (CAPD) and intermittent peritoneal dialysis. This complication was first reported by Gandhi et al. (1980) in the United States who described the appearance of marked sclerotic thickening of the peritoneal membrane in five patients on intermittent peritoneal dialysis for renal failure. Recently Holland (1990) has reported three additional cases. Sclerosing peritonitis is an inflammatory process leading to the deposition of a thick fibrous tissue membrane on the peritoneum. As the condition progresses, the mesentery also becomes thickened and contracted and as a result the small bowel is drawn up out of the pelvis and is trapped behind the thickened membrane. Eventually the small bowel becomes totally encapsulated, leading to acute or sub-acute small bowel obstruction. By January 1986, 68 cases of sclerosing peritonitis resulting from CAPD therapy had been documented in the Co-operative International Study (Slingeneyer, 1987) with the majority of cases occurring in Glasgow and three centres in France. No single causal agent has been identified but various factors such as the use of acetate containing dialysate solutions (Rottembourg et al., 1983) and the accidental introduction of the antiseptic chlorhexidine into the peritoneal cavity (Junor et al., 1985) have been implicated. The early clinical features of this condition are nonspecific and include colicky abdominal pain and progressive loss of ultrafiltration. If these prodromal phenomena are not recognized, the diagnosis may not be made until the patient develops acute intestinal obstruction necessitating surgery. At laparotomy, an attempt is usually made to free the small bowel loop from the constricting membrane, but only occasionally is it possible to identify a plane of cleavage between the small bowel and the membrane. An alternative approach is to make multiple releasing incisions in the thickened membrane to free the underlying bowel. The prognosis of sclerosing peritonitis is poor with Correspondence to: Dr A. S. Hollman, Department of Radiology, Western Infirmary, Dumbarton Road, Glasgow G11 6NT.

death usually occurring within a few weeks or months of surgery. The features of sclerosing peritonitis following practolol therapy, as seen on upper gastrointestinal barium studies, have been described by Lee et al. (1977), and are similar to those found complicating CAPD. Separation of fixed and dilated small bowel loops and delayed small intestinal transit are characteristic. However, the ultrasound features of sclerosing peritonitis in CAPD patients have not previously been fully documented.

P A T I E N T S AND M E T H O D S Over a 5 year period from February 1982 to June 1987, 17 patients in the Western Infirmary, Glasgow developed sclerosing peritonitis as a complication of CAPD. Fourteen of these patients have been examined by ultrasound and their findings are the subject of this report. The clinical details of these patients are summarized in Table 1. The patients were aged from 23 to 65 years (with a mean age of 47 years); six patients were male and eight female. All patients demonstrated similar clinical features with vague gastrointestinal symptoms initially, followed by acute or subacute small bowel obstruction requiring laparotomy. Most patients died either in the immediate post-operative period or later from cachexia as a result of malabsorption following extensive small bowel resection. Only four of the 14 patients have survived, all of whom received renal transplants with associated immunosuppressive therapy. We have reviewed the ultrasonic findings in these 14 patients. In all cases the patients were examined by one of two Consultants experienced in abdominal ultrasound using either the ATL MK100 or. Diasonics DRF400 real time systems. The Unirad EDP 1000 static system was used to document the changes pictorially. Latterly, all patients were examined with the dialysis fluid left in the abdomen, as this enabled the ultrasonic features to be more easily demonstrated. The stand-off technique has also proved useful in assessing the changes in the bowel occurring immediately beneath the anterior abdominal wall.

177

US CHANGES IN SCLEROSING PERITONITIS FOLLOWING CAPD

Table 1-Clinical

details

Case no. Age

Sex

Duration of at presentation (months)

CAPD Management

Outcome

Laparotomy. Died in post-operative period Laparotomy Post-operative prolonged ileus resulted in death Laparotomy_ Survived for 1 year. Died following laparotomy for recurrent obstruction Laparotomy. Died after 2nd laparotomy 1 year later Laparotomy for bowel obstruction. Received renal transplant and immunosuppressant drugs Laparotomy. Died in post-operative period Laparotomy. Died in post-operative period Successful renal transplant and immunosuppressive drugs. No surgery Laparotomy. Died post-operatively Haemodialysis after C A P D failed. Bowel obstruction developed several months later resulted in laparotomy. Died post-operatively Laparotomy. Prolonged ileus over weeks with eventual death Laparotomy. Urgent renal transplant received post-operatively. On immunosuppressants Laparotomy. Post-operative death Laparotomy. Renal transplant and immunosuppressive therapy. Short bowel syndrome

Died Died Died

1 2 3

59 49 46

F M F

58 37 24

4 5

54 30

M F

26 24

6 7

43 48

F M

8

23

M

9 l0

65 59

F F

71 5 36 5 23

11 12

55 25

M F

40 14

13 14

45 53

F M

24 24

Table 2-Ultrasonic

Case no.

Died Died Well Died Died Died Well 3 years later Died Alive 1 year. Malabsorption from short bowel syndrome

findings

Abdominal small bowel peristalsis

Tethering of bowel posteriorly .

Echogenicstrands

.

Membrane formation

Rapid progression on subsequent scans

1

.

2 3 4 5 6 7

+ + + + + --

+ + + + + -

+ -+ +

+ -+ + +

+ + -+ +

8 9

+

--

+

-

--

+ + + + + +

+ + + + +

+ + + -

+ -

10 11 12 13 14

Died Well 4 years later

.

+ + + -

Other features

Polycystic kidneys fill abdomen Polycystic kidneys

Inflammatory gut mass LUQ

+ / --, present/absent.

The scans and reports were re-examined and assessed for the following features: abnormal or increased small bowel peristalsis, tethering of bowel loops to the posterior abdominal wall, intraperitoneal echogenic strands, and the presence of the characteristic membrane demonstrated anteriorly over tethered bowel loops. Of these 14 patients, 10 had plain supine and erect abdominal radiographs performed on admission to hospital, and 9 of the 14 had a small bowel follow through examination performed, following ultrasonic assessment.

Tethering of bowel posteriorly occurred in 10 patients who had obvious tethering of bowel loops to the posterior abdominal wall. As the condition progressed the bowel loops became increasingly matted together, eventually

RESULTS The results of the ultrasonic examinations are summarized in Table 2. Abnormal small bowel activity was seen in 12 of the 14 patients. They had increased small bowel peristalsis (when assessed on a real time system). This affected several loops of small bowel, which also appeared dilated and fixed in position.

Fig. 1 - Case 5. Tethering of bowel posteriorly. Transverse scan of mid abdomen showing tethering of bowel loops (B) to the posterior abdominal wall.

178

CLINICAL RADIOLOGY

Fig. 2 Case 3. Echogenic strands. Sagittal scan of right upper abdomen. Note echogenie strands (arrows) in sub-hepatic space.

Fig. 3 Case 5. Membrane formation. Transverse scan of mid abdomen. Arrowheads demonstrate characteristic pre-visceral membrane.

with ascitic fluid lying in front of them, long after C A P D had been discontinued (Fig. 1). Intraperitoneal echogenic strands were demonstrated in seven patients. These strands were usually numerous and thin and in the early stages of the disease were most easily identified around the liver (Fig. 2). However, in the later stages, the strands could often be seen throughout the peritoneal cavity. Membrane formation was characteristic. This membrane lay anterior to the matted bowel and was demonstrated in five cases, all in the late stages of the disease. It appeared as a well-defined, flat, uniform echogenic layer whose thickness varied 1 to 4 m m (Fig. 3). Progression of disease took place in seven cases. There was rapid progression of the above changes demonstrated with ultrasound over a 12 month period as shown in Fig. 4(a) and (b). The plain abdominal radiographs were reported as being normal in five cases, showing small bowel obstruction in three patients and non-specific small bowel dilatation in the last two cases_ The small bowel follow through examinations were more informative than plain radiographs. In all nine cases there was a markedly delayed transit time through the small bowel, often exceeding 24 h. In seven patients, the small bowel loops failed to descend into the pelvis and there was obvious separation of rigid, fixed bowel loops. Small bowel dilatation was a less c o m m o n finding (five patients).

DISCUSSION

(a)

(b) Fig. 4 Case 11. Rapid progression of disease. Transverse scans of mid abdomen. (a) No features of sclerosing peritonitis seen at onset of symptoms. (b) Severe disease obvious 4 months later. Note posterior tethering of bowel (B), membrane formation (arrow), and widespread echogenic strands (arrowhead). Death occurred several weeks later.

The present study shows that ultrasound is a rapid and sensitive means of demonstrating the features of sclerosing peritonitis in patients with C A P D (Hollman et al_, 1988). The earliest and most c o m m o n finding was increased peristalsis affecting several bowel loops, although this was difficult to assess objectively. As the condition progressed, the bowel loops became increasingly tethered posteriorly (Figs 1 and 4(b)). Widespread fine intraperitoneal echogenic strands were seen throughout the development of the disease in the sub-phrenic and sub-hepatic spaces. These were most prominent and were more easily seen when dialysis fluid was present in the peritoneal cavity. The characteristic pre-visceral membrane which encased the tethered and matted bowel loops was demonstrated only in the late stages of the disease. It occurred in association with free peritoneal fluid lying anteriorly, and persisted long after C A P D had been discontinued (Figs 3 and 4(b))_ The evolution of these ultrasound features mirrored the progressive deterioration in the clinical condition of the patient. In only one of the 14 cases (case 1) were the characteristic features not identified due to the presence of grossly enlarged polycystic kidneys, which precluded assessment of other intraabdominal pathology. Abdominal radiographs were shown to be of little value in initiating a diagnosis, but the barium follow through examinations, although less sensitive, were certainly complementary to the ultrasonic assessment. The first patients in this series who developed sclerosing peritonitis were diagnosed relatively late in the disease process (case nos 2, 3, 4, 5, 11, 12 and 13) whereas those who developed the disease more recently were identified at an earlier stage. This reflected increased awareness by

US C H A N G E S IN S C L E R O S I N G P E R I T O N I T I S F O L L O W I N G C A P D

the clinicians o f this complication and earlier referral for imaging. Moreover, the development o f expertise in the technical methods o f demonstrating and recognizing the characteristic features probably led to earlier diagnosis. Cessation o f C A P D does not halt or reverse the progression o f sclerosing peritonitis, except perhaps at an early stage (Niaudet et al., 1987). However, the fact that our four survivors received renal transplants fairly soon after diagnosis suggests that the associated i m m u n o s u p pressive therapy m a y have had a beneficial effect on the course o f the disease_ Thus early diagnosis m a y be important in reducing the high mortality which has been reported as being 80% (Novello and Port, 1986). In conclusion, any patient receiving maintenance peritoneal dialysis, who presents with a history o f vague abdominal pain accompanied by loss o f ultrafiltration capacity o f the peritoneum, should be suspected o f having sclerosing peritonitis. Such patients should be investigated by means o f a barium follow t h r o u g h examination (Lee et al., 1977; N i a u d e t et al., 1987) and ultrasound. If these studies prove negative and symptoms persist, the examinations should be repeated after an interval o f several m o n t h s as the changes m a y then have become evident. Increased awareness o f this condition, both by the clinician and radiologist, is essential if treatment, which m a y prevent an otherwise fatal outcome, is to be instituted.

179

REFERENCES

Gandhi, VC, Humayun, HM, Ing, JS, Dangirdas, JT, Jablokow, VR, Iwatsuki, S et al. (1980). Sclerotic thickening of the peritoneal membrane in maintenance peritoneal dialysis patients. Archives of Internal Medicine, 140, 1201-1203. Holland, P (1990). Sclerosing encapsulating peritonitis in chronic ambulatory peritoneal dialysis. Clinical Radiology, 41, 19 23. Hollman, AS, McMillan, M & Morley, P (1988). Ultrasound changes in sclerosing peritonitis (Abstract). British Journal of Radiology, 61, 532. Junor, BJR, Briggs, JD, Forwell, MA, Dobbie, JW & Henderson I (1985). Sclerosingperitonitis--the contribution of cholorhexidine in alcohol. Peritoneal Dialysis Bulletin, 5, 101-105. Lee, REJ, Baddeley, H, Marshall, AJ & Read, AE (1977). Practolol peritonitis. Clinical Radiology, 28, 119-128. Niaudet, P, Berard, E, Revillon, Y, Lothon, M. & Broyer, M (1987). Sclerosing encapsulating peritonitis in children. Contributions to Nephrology, 57, 230-238. Novello, AC & Port, FK (1986). Sclerosing encapsulating peritonitis. International Journal of Artificial Organs, 9, 393 396. Rottembourg, J, Gahl, GM, Poignet, JL, Mertani, E., Strippoli, P, Langlois, Pet al. (1983). Severeabdominal complications in patients undergoing continuous ambulatory peritoneal dialysis. Proceedings of European Dialysis and Transplant Association, 20, 236-242. Slingeneyer, A (1987). Preliminary report on a Co-operative International Study on sclerosingencapsulating peritonitis. Contributions to Nephrology, 57, 239 247.