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Nov 18, 2014 - Sonography is often the imaging modality on which ret- roperitoneal lesions .... neum. In: Rumack CM, Wilson SR, Charboneau JW, eds. Diag-.
Abdom Imaging 23:103–106 (1998)

Abdominal Imaging q Springer-Verlag New York Inc. 1998

Retroperitoneal edema: sonographic mimic of retroperitoneal fluid collection Ronald H. Wachsberg, Sunita Singh-Panghaal Department of Radiology, University Hospital and New Jersey Medical School, 150 Bergen Street, Room C-320, Newark, NJ 07103, USA Received: 12 July 1996/Accepted: 4 September 1996

Abstract Background: The sonographic finding of an anechoic retroperitoneal abnormality suggests a fluid collection (e.g., abscess, urinoma, hematoma). Our study was performed to evaluate cases in which this sonographic finding appeared to be a manifestation of systemic edema. Subjects and Methods: Inpatient sonograms performed over a 40-month period were reviewed for the presence of anechoic areas suggestive of fluid collection in the retroperitoneum of the flank. Records of patients with such findings were reviewed for evidence of retroperitoneal abscess, urinoma, or hemorrhage, as well as for the presence and cause(s) of peripheral edema. Results: Of the 29 patients identified with sonographic findings suspicious for retroperitoneal fluid collection, 13 (45%) had no cause for and no clinical evidence of focal retroperitoneal collection. All 13 patients had peripheral edema attributable to hypoalbuminemia, congestive heart failure, overhydration, cirrhosis, and/or the systemic inflammatory response (multiple organ failure) syndrome. Resolution of the retroperitoneal abnormality following therapy for congestive heart failure was documented in one case, and CT scan confirmed retroperitoneal edema in another. Conclusion: Anechoic regions that represent edema can be seen on sonograms of the retroperitoneum in patients with conditions that cause edema in other regions. The possibility of edema mimicking a fluid collection should be particularly considered prior to invasive procedures in the retroperitoneum. Key words: Retroperitoneal edema—Congestive heart failure—Peripheral edema—Sonography—Retroperitoneum.

Correspondence to: R. H. Wachsberg

Sonography is often the imaging modality on which retroperitoneal lesions are first detected. This is particularly so in acutely ill patients, for whom a portable imaging technique is often required. Differential considerations for focal echo-poor abnormalities noted sonographically in the retroperitoneum include fluid collections such as abscess, liquefied hematoma, extravasated urine, or pancreatitic inflammatory exudate [1]. Particularly when noted on sonograms in acutely ill patients, the suspicion of a retroperitoneal fluid collection may lead to invasive diagnostic and therapeutic intervention. We encountered a patient in whom sonography revealed a focal anechoic retroperitoneal lesion that mimicked a fluid collection but resolved following therapy for congestive heart failure (CHF). We speculated that the sonographic finding represented edema rather than one of the aforementioned fluid collections. To further assess this phenomenon, we performed a retrospective study of anechoic retroperitoneal abnormalities noted on sonograms performed over a 40-month period.

Materials and methods From a retrospective search of inpatient sonograms performed between January 1993 and May 1996, we identified all patients in whom one or more anechoic regions were noted in the retroperitoneum of the flank adjacent to the kidneys. Patients with sonographic retroperitoneal abnormalities in or near the midline but not in the flank were excluded. Sonograms had been performed with Acuson 128 or Toshiba SSA-140 scanners using a 2.0- to 5.0-MHz sector or curved array probes. Imaging studies and medical records of these patients were retrospectively reviewed to identify the cause of the retroperitoneal sonographic abnormalities. Specifically, we sought evidence of urinary obstruction, renal or perirenal infection, trauma, pancreatitis, congestive heart failure, cirrhosis, and hypoalbuminemia. Normal serum albumin concentration in our laboratory is ¢3 gm/dl, and we classified hypoalbuminemia as mild (2.5–2.9 gm/dl), moderate (2.0–2.4 gm/dl), or severe (below 2.0 gm/dl). The study was approved by the Institutional Review Board.

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R. H. Wachsberg and S. Singh-Panghaal: Sonography of retroperitoneal edema

Table 1. Thirteen patients (listed in alphabetical order) in whom one or more anechoic areas mimicking fluid collection were noted on retroperitoneal sonography Patient

Age

Sex

Cause(s) of edema

Underlying disease(s)

No. of sides involved

Serum albumin (gm/dl)

1

40

F

Hypoalbuminemia

Nephrotic syndrome

1

1.0

2

78

F

CHF

Cardiomyopathy

2

3.2

3

43

F

CHF, hypoalbuminemia

Diabetic nephropathy

1

1.9

4

38

M

Cirrhosis, hypoalbuminemia

Cirrhosis

1

2.2

5

49

F

SIRS

Cardiac arrest followed by SIRS

1

2.4

6

31

M

Hypoalbuminemia

AIDS-associated nephropathy, cryptococcal meningitis

2

0.9

7

21

M

Hypervolemia

Rhabdomyolysis due to cocaine

1

2.7

8

66

M

Cirrhosis, hypoalbuminemia

Cirrhosis

2

2.3

9

45

M

SIRS, CHF, hypoalbuminemia

Traumatic rhabdomyolysis followed by CHF and SIRS

2

2.6

10

51

M

CHF

Cardiomyopathy

1

2.5

11

48

F

CHF

Cardiomyopathy

2

3.1

12

56

F

SIRS

Aplastic anemia, gram-negative sepsis, but negative urine culture and urinalysis

2

3.8

13

41

M

Hypoalbuminemia

AIDS-associated nephropathy, pneumococcal pneumonia

1

1.7

Abbreviations: SIRS Å systemic inflammatory response syndrome; CHF Å congestive heart failure; AIDS Å acquired immune deficiency syndrome

Results We identified 29 patients in whom one or more anechoic regions suggestive of fluid were noted on sonograms of the retroperitoneum adjacent to the kidney. In most (if not all) cases, the abnormality appeared to be in the perirenal space, but precise localization was difficult to confirm, as the Gerota and Zuckerkandl fasciae were rarely seen. Previously reported causes (e.g., abscess, hematoma, urinoma) for the sonographic abnormality were diagnosed in 16 patients (55%); no such cause was identified in the remaining 13 patients (45%). Specifically, there was no evidence of urinary infection to suggest perirenal abscess, no evidence of urinary obstruction to suggest urinoma, no evidence of trauma, tumor, or coagulopathy to suggest hemorrhage, and no elevation of serum amylase to suggest pancreatitis. Each of these 13 patients had clinically evident peripheral edema due to various causes (Table 1). Congestive heart failure was the sole cause of peripheral edema in three cases and was present in five cases overall. Repeat sonography in patient 10 following medical therapy documented disappearance of an anechoic retroperitoneal abnormality concurrent with improvement in pedal edema, suggesting that the

retroperitoneal abnormality had also represented edema (Fig. 1). Edema in the retroperitoneum was also confirmed in patient 11, in whom computed tomography (CT) scan showed water density (5 Hounsfield units) in the normally fatty perirenal and pararenal spaces. Hypoalbuminemia was present in 10 cases (mean, 2.3 gm/dl; SD, 0.8; range, 0.9–3.8). The degree of hypoalbuminemia was graded as mild in three patients, moderate in three, and severe in four. Severe hypoalbuminemia was the sole identified cause of peripheral edema in three patients with nephrotic syndrome (Fig. 2). In the other seven patients, hypoalbuminemia coexisted with at least one other cause of edema. Two such patients had cirrhosis with portal hypertension accompanying moderate hypoalbuminemia. Systemic inflammatory response syndrome (SIRS) was the sole apparent cause of edema in two cases and was present in three cases overall. Patient 5 had SIRS following cardiac arrest and developed a unilateral fluid collection confirmed with CT scan which resolved over several days, without evidence of systemic infection or urinary tract pathology. Patient 12 with SIRS due to sepsis had bilateral perirenal fluid collections but normal urinalysis and urine culture, and without evidence of urinary obstruction.

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R. H. Wachsberg and S. Singh-Panghaal: Sonography of retroperitoneal edema

Fig. 1. Fifty-four-year old man with congestive heart failure and peripheral edema (patient 10). Sagittal (A) and transverse (B) sonograms show anechoic area (arrows ) in retroperitoneum posterior to upper pole of right kidney (k). No corresponding abnormality was seen on the left side. Following medical therapy and clinical improvement, repeat sonography 4 days later documented resolution of this finding, suggesting that the abnormality represented edema from cardiac congestion. e Å pleural effusion; h Å liver; c Å inferior vena cava.

In one case, pulmonary arterial catheterization confirmed that hypervolemia following aggressive hydration was the cause of peripheral edema and retroperitoneal fluid accumulation. In seven cases (54%), the anechoic retroperitoneal abnormality was unilateral versus six cases (46%) in which it was bilateral. All unilateral collections noted were on the right side.

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Fig. 2. Forty-year-old woman presenting with anasarca who was found to have serum albumin concentration of 1.0 gm/dl and proteinuria in the nephrotic range (patient 1). Sagittal (A) and transverse (B) sonograms reveal anechoic perirenal space (arrows) surrounding lower pole of right kidney (k ). Note characteristic cone-like configuration of perirenal space with apex directed caudally. Similar appearance was noted on the left side. h Å liver; p Å psoas muscle.

Discussion We have described 13 patients in whom anechoic regions noted on sonograms of the retroperitoneum appear to have been due to edema. The appearance of these areas was indistinguishable from that of fluid collections such as abscesses, hematomas, and urinomas. Particularly since several of the patients were acutely ill, the

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R. H. Wachsberg and S. Singh-Panghaal: Sonography of retroperitoneal edema

sonographic findings might have led to intervention for suspected retroperitoneal abscess. Edema can be caused by increased hydrostatic pressure, decreased oncotic pressure, and abnormal vascular permeability [2]. Retroperitoneal edema has been described in patients subjected to rapid vigorous fluid rescuscitation following blunt trauma [3], analogous to patient 7 in our series in whom hypervolemia was due to overhydration. Investigators have also noted abnormally high attentuation of retroperitoneal fat on CT scans of cirrhotic patients [4], analogous to our two cirrhotic patients. Congestive heart failure, hypoalbuminemia, and SIRS (also known as multiple organ failure syndrome) are other conditions in which peripheral edema is well known to develop, although retroperitoneal edema in these states has not been previously described on imaging studies, to our knowledge. Diffuse edema of the retroperitoneal tissues is frequently noted at laparotomy in patients with SIRS [5]; the underlying mechanism is thought to be abnormal vascular permeability caused by circulating chemical mediators [6, 7]. No patient in our series was evaluated with percutaneous aspiration or histopathological examination of the retroperitoneal sonographic abnormality; however, circumstantial evidence supports our impression that the sonographic abnormalities represented retroperitoneal edema in these cases. CT scan in patient 11 confirmed diffusely edematous retroperitoneal fat bilaterally. Sonography in patient 10 documented resolution of a retroperitoneal collection following medical therapy for CHF. No known cause of perinephric collection could be identified in any of the 13 cases. We cannot exclude the possibility that one or more cases we describe represented hypoechoic retroperitoneal fat, an occasional normal variant [8], but this is not likely to have been so in all patients. We were also careful to distinguish between perirenal fluid and a subcapsular hypoechoic cortical rim that has rarely been observed [9]. We do not know if the high prevalence of edema that we noted as the cause of retroperitoneal hypoechoic abnormalities represents its true prevalence. Based on

referral patterns at this institution, we suspect that those patients most likely on clinical grounds to harbor retroperitoneal collection might have been referred for CT scan instead of sonography. It is noteworthy that 54% of cases of retroperitoneal edema we noted were unilateral, contrary to the intuitive assumption that a systemic process is bilateral. Since unilateral findings were only observed on the right side, we speculate that edema may have been present but undetected in the left flank, which is technically more difficult to image sonographically. In summary, the sonographic finding of an anechoic area in the retroperitoneum can be a manifestation of systemic edema. In patients with peripheral edema, retroperitoneal edema should be included in the differential diagnosis of anechoic sonographic abnormalities in the retroperitoneum. In particular, the possibility of edema mimicking a fluid collection should be considered prior to invasive procedures in the retroperitoneum. References 1. Kriegshauser JS, Carroll BA. The adrenal glands and retroperitoneum. In: Rumack CM, Wilson SR, Charboneau JW, eds. Diagnostic ultrasound. St. Louis: Mosby, 1991:289–314 2. Guyton AC, Hall JE. Textbook of medical physiology, 9th ed. Philadelphia: WB Saunders, 1996:309–310 3. Chamrova Z, Shanmuganathan K, Mirvis SE, Erb RE. Retroperitoneal fluid resulting from rapid intravascular rescuscutation in trauma: CT mimic of retroperitoneal injury. Emerg Radiol 1994; 1:85–88 4. Tyrrel RT, Montemayer KA, Bernardino ME. CT density of mesenteric, retroperitoneal, and subcutaneous fat in cirrhotic patients: comparison with control subjects. AJR 1990;155:73–75 5. Livingston DH. Personal communication, July 1996 6. Demling R, LaLonde C, Saldinger P, Knox J. Multiple-organ dysfunction in the surgical patient: pathophysiology, prevention and treatment. Curr Prob Surg 1993;4:345–414 7. Cerra FB. Multiple organ failure syndrome. Dis Mon 1992;38: 843–895 8. Brammer HM, Smith WS, Lubbers PR. Septated hypoechoic perirenal fat on sonograms: a pitfall in renal ultrasonography. J Ultrasound Med 1992;11:361–363 9. Slater SP, Heller CA, Nanra RS, Jones WS. The hypo-echoic cortical rim in lupus nephritis. Australas Radiol 1994;38:46–47

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