Acute extraperitoneal infection

Acute

Extraperitoneal

Infection

Morton A. Meyers, M.D.

R

ECENT CLARIFICATION of the radiologic anatomy of the extraperitoneal spaces now permits ready identification, localization, even pinpointing the precise site of origin of most extraperitoneal abscesses. This is particularly important in view of the clinically occult nature of these lesions. Extraperitoneal tissues do not react as acutely and severely to bacterial contamination as does the peritoneal cavity. I2 Known amounts of bacteria introduced intraperitoneally result in acute peritonitis and dramatic constitutional signs. When introduced into the extraperitoneal tissues, however, they cause a more smoldering infection. This explains the prolonged duration of the symptoms of extraperitoneal abscess prior to operation or death, often as long as 2 mo. 24 Several reports emphasize the difficulties in clinically recognizing even severe extraperitoneal infection. Indeed, in large series, the diagnosis has been completely overlooked in 25”,/,-50% of the patients. ‘.24 The area is not accessible to. the bedside modalities of auscultation, palpation, or percussion. Unless diagnosed early and treated adequately, extraperitoneal abscess is associated with prolonged morbidity and high mortality. ’ It is apparent that the radiologist is in a position to be the first to make the diagnosis. Altemeier and Alexander, in their review of 189 patients with proved extraperitoneal abscess, emphasized that 90y0 of those who had roentgen examination showed significant abnormalities. ’ Welin established the radiologic diagnosis of perirenal abscess in 17 patients, including eight in whom the process was clinically unsuspected. 26 It is essential to realize that the extraperitoneal space is not, as an editorial has woefully designated it, an amorphous “hinterland of straggling mesenthyme with . . shadowy fascial boundaries.” I9 Rather, recent roentgen- anatomic studies have clarified the fascial relationships that clearly demarcate the region into three distinct compartments. I2 Each has specific boundaries and relationships that can be recognized radiologically. Margination and extension of the infection within a particular extraperitoneal compartment are guided primarily by the fixed fascial planes and paths of least resistance. Extraperitoneal infection is usually secondary, a complication of infection, injury, or malignancy of adjacent retroperitoneal or intraperitoneal organs. Only rarely is it a consequence of bacteremia or suppurative lymphadenitis. Basic to an understanding of the radioiogic criteria is precise knowledge of the anatomy of the extraperitoneal fascial planes, compartments, and relationships. ANATOMIC CONSIDERATIONS The extraperitoneal space is clearly divided into three compartments: (I) the anterior pararenal space, (2) the perirenal space, and (3) the posterior pararenal Morton A. Meyers, M.D.: Deparrmenr of Radiology, Megical Center, New York, N. Y. 10021. fi lY;‘3 hv Grune & Stratton.

.Semmars

,n Roentgenology,

The New York Hospital-Cornell

L’niversir,~

Inc.

Vol VIII. No. 4 (October).

1973

445

MORTON

Fig. 1. (A) Extraperitoneal muscle; black arrowheads, black arrows, anterior and terior pararenal fat; f, flank sion of Radiology,‘*) (6; renal space; 2. the perirenal

A. MEYERS

anatomy of the right flank. K, kidney; C. ascending colon; Pm, psoas posterior parietal peritoneum: white arrowheads, transversalis fascia; posterior renal fascial layers; white arrows, lateroconal fascia; p, pos(properitoneal) fat. (From Meyers MA, at al; reproduced with permisopposite page) The three experitoneal spaces. 1. the anterior paraspace; 3, the posterior pararenal space.

space. Their margination is provided by distinct fascial in Fig. lA, which is a horizontal cross section through from behind. The extraperitoneal region extends from the posterior front to the transversalis fascia posteriorly. Central to

layers. These are shown the right flank, viewed parietal peritoneum in its division are the an-

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INFECTION

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terior and posterior layers of renal fascia (Gerota’s fascia),’ which envelop the kidney and perirenal fat. Two conspicuous anatomic features have particular clinical significance: (1) perirenal fat is most abundant posterior and somewhat lateral to the lower pole of the kidney, and (2) the two renal fascia1 layers fuse behind the ascending or descending colon to form the single lateroconal fascia, which then blends with the peritoneum. Behind the posterior renal fascia is another thinner layer of fat. It continues laterally behind the lateroconal fascia where it is visualized as the properitoneal fat of the “flank stripe.” Figure IB diagrams the three extraperitoneal compartments, demarcated by the lines of fusion of these fascial layers. The anterior parurenaf space extends from the posterior parietal peritoneum to the anterior renal fascia. It is confined laterally by the lateroconal fascia. The perirenal space encompasses the kidney and its investing fat. The posterior parurenal space is the thinnest, extending between the posterior renal fascia and the transversalis fascia. It continues laterally external to the lateroconal fascia as the flank fat. Figure 2 more comprehensively illustrates these relationships. The. anteriorpararenal space includes the ascending and descending colon, the entire duodenal loop, and the pancreas. While it is potentially continuous across the midline, fluid collections within it may not spread to the opposite side,” but rather drain inferiorly toward the iliac fossa and pelvis. Pancreatitis is an exception to this rule, and commonly spreads bilaterally. The perirenaf compartments have no continuity across the midline. Medially, the posterior renal fascia fuses with the strong psoas or quadratus lumborum

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Fig. 2. Relationships and structures of the three extraperitoneal spaces. (A) Horizontal diagram. (B) Left parasegittal diagram: L. liver; K. kidney; P. pancreas: C. descending colon.

ACUTE

EXTRAPERITONEAL

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Fig. 3. Schema of extraperitoneal fat layers contributing to radiographic visualization of the psoas muscle. On the left, the cone of renal fascia has been cut to identify its two layers enclosing the perirenal space overlying the psoas muscle. On the right, the horizontal diagrams, viewed from the beck, indicate the major fat interfaces of the psoas muscle at different levels. PM. psoas muscle; K, kidney; C, colon.

fascia,’ and the anterior renal fascia blends into the dense mass of connective tissue surrounding the great vessels. I3714There are, then, two perirenal spaces with no actual or potential communication. 12-r4 The l,ines of fusion of the anterior and posterior renal fascial layers are unique and distinctly contribute to the spread and confinement of extraperitoneal infection. The perirenal space on each side narrows as it extends inferiorly (Figs. 2B and 3) resembling an inverted cone. * Inferiorly, the layers fuse weakly or blend with the iliac fascia; as they narrow medially, they also blend loosely with the periureteric connective tissue. Although the apex of the cone is anatomically open toward the iliac fossa, most infections are confined to the perirenal space by early inflammatory sealing of this potential outlet. Sections through the extraperitoneal tissues at different levels have clarified the radiographic anatomy of the psoas muscle (Fig. 3). At the level of the kidney, the psoas muscle border is visualized by virtue of the contrast provided by perirenal fat. However, below the kidney, the psoas muscle outline is seen because of posterior pararenal fat. Infection limited to one compartment can therefore be further localized radiologically by recognizing segmental loss of the psoas shadow. The posterior pat-arena1 space is demarcated on each side of the body by the fusion of the transversalis fascia medially with the muscle fascia. The space is open laterally toward the flank and inferiorly toward the pelvis. *For this reason, the single layer of fascia extending has been designated as the lateroconal fascia.4

laterally

from the cone of renal Fascia

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Two anatomic features have particular diagnostic significance in the region of the iliac fossa below the cone of renal fascia: (1) the anterior and posterior pararenal spacesare here in potential communication (Fig. 2B), and (2) at this level, the lateroconal fascia disappears as a distinct boundary so that the anterior pararenal space communicates laterally with the properitoneal fat of the flank stripe. PATHWAYS

OF FLOW OF EXTRAPERITONEAL

INFECTION

The distribution and localization of extraperitoneal fluid within the three compartments have been radiographically studied by injecting contrast medium in adult cadavers. ‘*These have clarified not only the pathways of flow but also the roentgen diagnostic criteria of extraperitoneal infection. The anteriorpararenaf space is opacified in Fig. 4. It is apparent that the long axis of the density is vertical. Flow laterally is limited by the lateroconal fascia

Fig. 4. Postmortem injection oi f anterior is mainpararenal space. The flank stripe tained (arrowheads). Extension into the triangular ligament of the liver has occurred (arrows).

ACUTE

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so that the hank stripe is preserved. The hepatic or splenic outline, displaced from its bed of contrasting extraperitoneal fat, is lost. Superiorly, on the right. communication is established across the reflections of the triangular ligament ot the liver (Fig. 4). The occasional development of abscess in the bare area of the liver secondary to extraperitoneal infection, most commonly from appendicitis, is explained by this anatomic continuity with the anterior pararenal space. The perirenal space is opacified in Fig. 5. The introduction of successive increments of contrast medium demonstrates that at first the fluid is evenly dispersed throughout the perirenal fat. Preferential flow then seeks the abundant fat dorsolateral to the lower pole of the kidney. Distension of the perirenal space yi,elds a characteristic outline. The lower border of the distended cone ol renal fascia presents a diagnostic silhouette, inferiorly convex over the iliac crest. The axis of the fluid density is vertical. The weakest point, through which perirenal effusion escapes most easily. is at the inferomedial angle of the perirenal space adjacent to the ureter I3 (Fig. 5). With greatly increased pressure in the perirenal space, transperitoneal rupture may occur in the region of the renal hilum. “J’ The posterior pararenal space is opacified in Fig. 6. The natural spread is inferiorly and laterally, and this is reflected by the axis of the fluid density.

Fig. 5. Postmortem injection of perirenal space. The distended space shows a convex border inferiorly. overlying the iliac crest (arrows). A small amount of contrast medium has escaped around the ureter. (From Meyers MA et al; re ro14 ) duced with permission of Radiology.

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Fig. 6. Postmortem injection of posterior pararanal space. Medially the collection parallels the psoas muscle (large arrows). Laterally, there is extension into the flank fat (small arrows). (From Meyers MA, at al; reproduced with permission of Radiology.“)

Medially, the collection is limited by and therefore parallels the margin of the psoas muscle. The psoas shadow itself, however, is obliterated. Lateral spread extends into and obliterates the flank stripe. The kidney outline and perirenal fat shadows tend to be preserved. CLINICAL

CONSIDERATIONS

The predominant symptoms of an extraperitoneal infection are chills, fever, abdominal or flank pain, nausea, vomiting, night sweats, and weight loss. The clinical course is usually insidious and the initial symptoms are so nonspecific that the correct diagnosis is usually not considered. With pressure on the extraperitoneal nerves, pain may be referred to the groin, hip, thigh, or knee with little or no complaint of abdominal or back pain. ’ Urologic symptoms are rare even with perirenal abscess.24

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A mass or swelling of the flank is palpable in about SO%,’ but only if large or if it localizes inferiorly below the costal margin. Almost all patients exhibit tenderness to palpation over the abscess. Scoliosis, psoas spasm, and a sinus tract may be other clinical signs. Although there is invariably leukocytosis, urinalysis may be normal, even in perirenal abscess. The most common complications of extraperitoneal abscessinclude rupture into the free peritoneal cavity and progressive dissection in the soft tissues. Spread may involve the anterior abdominal wall, subcutaneous tissues of the back or flank, subdiaphragmatic space, mediastinum, thoracic cavity, psoas muscle, thigh, or hip. A fistula may extend from the kidney into the extraperitoneal portion of the bowel or into a bronchus. ROENTGEN

FINDINGS

The detection and localization of an extraperitoneal infection depends on its effacement of normal extraperitoneal contrast landmarks and its effect on extraperitoneal organs. Coned-down studies of plain films or intravenous pyelograms, and supplemental lateral views on barium contrast studies may be particularly helpful. The hallmark of extraperitoneal gas is a collection of mottled and linear radiolucencies that often track along established fascial planes. On erect or decubitus films, the gas remains fixed in position, a reliable distinction from intrape:ritoneal gas. Only rarely are circumscribed air-fluid levels identifiable. Anterior Pararenal Space Abscess

This is the most common site of extraperitoneal infection. Of 160 patients with extraperitoneal abscess,the process was confined to the anterior pararenal space in 84 (52.5%).’ Most arise from primary lesions of the alimentary tract, especially the colon, appendix, pancreas, and duodenum. The primary radiologic criteria for localization in this space are summarized in the first column in Table 1. Table

1. Extraperitoneal

Abscess-Localizing

Antemr Roentgen Perrrenal

fat

Feature and

renal

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space

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Preserved

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Preserved

Preserved

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Oblrterated

Preserved

Anterror

Anterror

or duodenoJunctron

stripe

Hepatrc

and

colon of descending

duodenum

Anterror

lateral. superror

and

splemc

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or

MORTON

A. MEYERS

Fig. 7. Anterior pararenal space absces is from gra se\ lomatous ileocolitis. (A) Barium enema Ivveals (EJ Obstl ilaoileal, ileocolic, and colocolic fistulas. tion of the right ureter secondan/ to the (sxtraperitor infect.ion.

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Localized obstruction with hydronephrosis may be produced by pressure on the ureter below the cone of the renal fascia. Extraperitoneal abscess may result from perforated carcinoma or diverticulitis of the colon, or granulomatous ileocolitis with extension of infection into the extraperitoneal tissue’,*’ (Fig. 7). The latter characteristically occurs on the right side at the level of L4 or L5. In children particularly, it may develop secondary to appendicitis. Surprisingly large abscesses may develop. Because the structures deep to the anterior pararenal space are relatively unyielding, a massive accumulation of exudate tends to distend it anteriorly toward the peritoneal cavity. This may bring the collection into contact with the mesenteric portion of the bowel. Figure 8 illustrates a huge extraperitoneal abscess due to appendicitis causing secondary inflammatory effects upon the proximal transverse colon. Extraperitoneal spread of a pancreatic abscess may be extensive but usually follows recognizable planes. Drainage from the head of the pancreas tends to be downward and to the right. The pancreatic infection may then come into contact with the ascending colon. Associated extraperitoneal fat necrosis may result in colon structure simulating primary carcinoma. ” Figure 9 clearly illustrates such a collection and the pathway of spread.

Fig. 8. Large anterior pararenal space abscess originating from appendicitis (note deformity of the medial contour of the cecum) and extending to the transverse colon. (Courtesy of Dr. AS Berne. Grouse-Irving Memorial Hospital, Syracuse. NY.)

MORTON

A. MEYERS

Fig. 9. Abscess of head of pancreas extending into right space. anterior pararenal (A) Drainage to the distal ascending colon produces an annular constricting lesion simucarcinoma lating primary Postoperative (arrow). (9) upper GI series clearly demonstrates the pathway of spread of the pancreatic infection. A sinus tract and pocket 6). originating from the third portion of the duodenum, extends downward and to the right to the area of colonic involvement.

Medially, some demarcation of the pancreatitis may be provided by the line of attachment of the small bowel mesentery. Infection arising from a penetrating ulcer or traumatic rupture of the duodenum, or pancreatic abscess is generally restrained from the flank fat by the lateroconal fascia. Only when it progresses inferiorly below the apex of the cone of renal fascia and the limitation of the lateroconal fascia can the infection proceed directly to the pro-

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Fig. 10. Pancreatitis secondary to duodenal ulcer. The anterior pararenal extension reaches the flank fat external to the peritoneum below the level of the cone of the renal fascia. (From Wulsin JH: reproduced with permission of Surg Gynecol Obstet.*’ )

peritoneal fat (Figs. 10 and 11). Gaseous lucencies may then be identified in the extraperitoneal tissues with local extension into the Rank stripe at the level ot the iliac crest and cephalad (Fig. 11). Violation of the fascial boundaries in cases of blunt retroperitoneal duodenal rupture may result in gas surrounding the right kidney.‘j This has been observed in four of 12 patients studied radiographically. Emphysema in the transverse mesocolon is also reported. 9125Serial roentgenograms and laminagraphy may clarify this subtle finding and distinguish it from colonic content. Upper GI series with water-soluble contrast medium may demonstrate the perforation site (Fig. 1 IA). Suppurative lymphadenitis may involve the nodes of the anterior pararenal space. Lymphangiography may demonstrate impression upon the duodenum by such enlarged retroperitoneal lymph nodes. 2’ Perirenal

Space Abscess

The overwhelming majority of perirenal abscesses are secondary to a renal infection. The underlying condition is commonly pyelonephritis, pyonephrosis,

MORTON

A. MEYERS

Fig. 11. Extraperitoneal perforation of the descending duodenum following blunt trauma with anterior pararenal space infection. (A) Gastrografin 01 series shows extravasation from the duodenum. Mottled gaseous lucencies extend inferiorly and laterally. Below the level of the cone of the renal fascia and the lateroconal fascia, the infection reaches and then ascends the flank fat (arrows). (Courtesy of Dr. AS Berne. Crouse-Irving Memorial Hospital, Syracuse, NY.) (B) Diagram of the pathway of spread inferior to the lateroconal fascia to communicate with the flank fat.

tuberculosis, or carbuncle. ’ Perforation of the capsule then leads to contamination of the perirenal space. Two predominant forms may be encountered. An acute gas producing infection can diffusely involve the perirenal compartment. It is secondary to E. coli, Aerobacter aerogenes or, rarely, Clostridium, and develops especially in diabetics. The gas may encircle the kidney or present as a mottled localized collection of radiolucencies within the shadows of the perirenal fat. Three characteristic roentgen features further localize the infection to the perirenal space: (1) associated exudate distends the cone of the renal fascia so that its lower border can be identified as an inferiorly convex shadow overlying the iliac crest (Fig. l2A); (2) the gas is most prominent within the rich fat posterior to the kidney (Fig. 12B); and (3) inflammatory thickening of the renal fascia itself may be seen(Fig. l2B). Fluid levels may be identified in the upright position.2 Subsequent to diffuse contamination of the space, the infection typically localizes in the most abundant portion of perirenal fat, posterior and

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Fig. 12. Acute gas producing left perirenal abscess. (A)S,ln addition to the mottled radiolucencies, fluid distension of the renal fascial cone overlies the iliac crest, presenting a typical convex inferior border farrows). (From Meyers MA. et al; reproduced with permission of Radiology.“I (E j Oblique view demonstrates preponderance of the gas and fluid in the perirenal fat dorsal to the kidney. Inflammatory thickening of the anterior renal fascia is shown as a curvilinear density (arrowheads).

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Fig. 13. Right perirenal abscess. The infection is localized behind the lower pole, resulting in anterior, medial, and superior displacement of the kidney. (A) The affected kidney appears larger because of the magnification resulting from its anterior displacement. There is loss of the renal outline and the hepatic angle. Extension of the infection along the ureter has caused mild ureteropelvic ob. struction. (6) On oblique projec tion, the abscess itself is visual.

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somewhat lateral to the lower pole of the kidney. The infection is guided by gravity along the path of least resistance. The major radiologic signs of a coalescent perirenal abscessare summarized in the sec:ondcolumn in Table 1. The kidney is usually displaced medially and upward, and may be rotated about its vertical axis. Pushed forward, the kidney appears larger on frontal films because of magnification (Figs. 13A and 14). Even though there is loss of the renal contour, the outline of the abscessmass itself may be visualized (Fig. 13B). Extrinsic compression of the renal pelvis and proximal ureter may also be present (Fig. 13A). Intravenous or retrograde pyelography often demonstrates gross disease of the collecting system and, at times, extravasation into the perirenal space. Fulminating infection may disrupt the perirenal fascial boundaries and spread diffusely into the iliac fossa (Fig. 15) or anteriorly to involve the bowel. Fixation of the kidney on erect views or during respiration is often present. Nesbit and Dick showed that of 85 patients with perirenal abscesses,14 (16.59,;) had supraphrenic complications. I6 These ranged from mild pleuritis with restriction of diaphragm motility and pulmonary basilar changes to nephrobronchial fistula. Posterior Pararenal Space Abscess

Infection limited solely to this compartment is rare. The posterior pararenal space itself includes no organs from which infection can directly arise. Except for the unusual case consequent to bacteremia, infection here develops as a complic:ation of osteomyelitis of the vertebral column or twelfth rib. ’ Abscess behind the transversalis fascia is not, strictly speaking, extraperitoneal: but retrofascial abscess (largely of osseous origin from infection in the spine or twelfth rib, often from tuberculosis or actinomycosis) may occasionally trans-

Fig. placing sulting matory

14. Large left perirenal abscess disthe lower pole anteromedially and rein renal magnification. Gross inflamdisease involves the collecting system.

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Fig. 15. Extensive perirenal abscess draining into the iliac fossa beyond the confines of the renal fascia. The abscess originated from a lower balyx (arrow) in a kidney involved by severe pyonephrosis. Retrograde pyelogram. (From Nagamatsu GR: reproduced with permission of Lippincott co.-)

gress fascial planes to involve the posterior pararenal space. Fulminating perirenal infection rarely does this. Table 1, column 3 summarizes the roentgen findings in diffuse involvement of the posterior pararenal space. The natural direction of extension is inferior and lateral, paralleling the outline of the psoas muscle but completely obliterating it. The lower pole of the kidney tends to be displaced laterally as well as anteriorly and upward. The hallmark of lateral extension in the posterior pararenal space is encroachment upon, and then obliteration of the flank stripe. We have noted an interesting extension of infection to the posterior pararenal

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Fig. 16. Pancreatic extravasation with extension down the anterior pararenal space and then upward into the posterior pararenal compartment. (A) Plain film shows a soft tissue mass. There is loss of the psoas shadow and lateral displacement of the descending colon with loss of the flank stripe. (B) Contrast injection into the collection via a drainage tube verifies its spread to the posterior pararenal space. (C) Diagram of the pathway of spread around the apex of the perirenal space. P. pancreas; K. kidney.

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space from the anterior pararenal space without contamination of the intervening perirenal compartment. This has occurred in three patients who had pancreatitis with extravasation. The process spreads from the pancreas down the anterior pararenal space and then rises posterior to the cone of the renal fascia within the posterior pararenal space (Fig. 16). The kidney and colon are pushed forward and the psoas muscle and flank stripe obliterated. This pathway provides an explanation for the subcutaneous discoloration of the flank (Turner’s sign) and periumbilical region (Cullen’s sign) in severe pancreatitis. REFERENCES tions of the kidney, in Friedenberg RM (ed): 1. Altemeier WA, Alexander JW; RetroperiRadiographic Atlas of the Genitourinary Systoneal abscess.Arch Surg 83512-524, 1961 tem. Philadelphia, Lippincott, 1966 2. Braman R, Cross RR Jr: Perinephric 16. Nesbit RM, Dick VS: Pulmonary comabscess producing a pneumonephrogram. J plications of acute renal and perirenal supUral 75194, 1956 puration. Am J Roentgenol44:161-169, 1940 3. Britt LG, Wolf RY: Postbulbar ulcer with 17. Neuhof H, Arnheim EE: Acute retroretrocecal abscess: a case report. Arch Surg peritoneal abscess and phlegmon: study of 65 92:98-100, 1966 cases.Ann Surg Il9:74l-758, 1944 4. Congdon ED, Edson JN: The cone of 18. Parks RE: The radiographic diagnosis of renal fascia in the adult white male. Anat Ret perinephric abscess.J Urol 64:555, 1950 80:289-313, 1941 19. Periureteric fibrosis. Lancet 2:780-781. 5. Evans JA, Meyers MA, Bosniak MA: 1957 Acute renal and perirenal infections. Semin 20. Rabinowitz JG, Present DH, Banks PA, Roentgen01 6:274-291, 1971 6. Gerota D: Beitrlge zur Kenntnis des et al: The roentgenographic features of ureteral obstruction ’ secondary to granuBefestigungsapparates der Niere. Arch Anat lomatous disease of the bowel. Clin Radio1 Entwcklngsgesch 2655286, 1895 22:205-209, 197I 7. Ginzburg L, Oppenheimer GD: Urologi21. Renert WA, Hecht HL: Lymphangiocal complications of regional ileitis. J Urol graphic demonstration of impression upon the 59:948-952, 1948 8. Hashmonai M, Abramson J, Erlik D, et duodenum by retriperitoneal lymph nodes. Br J Radio1 44:189-194, 1971 al: Retroperitoneal perforation of duodenal 22. Skarby HG: Beitrlge zur Diagnostik der ulcers with abscess formation. Ann Surg 173: Paranephritiden mit besonderer Berucksichti409,197l gung des Rontgenverfahrens. Acta Radio1 9. Jacobs EA, Culver GJ, Koening EC: Suppl62:1-165, 1946 Roentgenologic aspects of retroperitoneal per23. Sperling L, Rigler LG: Traumatic retroforations of the duodenum. Radiology 43: peritoneal rupture of duodenum: description of 563-57 I, 1944 valuable roentgen observation in its recogniIO. Meyer HI: The reaction of retroperitoneal tissue to infection. Ann Surg 99:246-250, tion. Radiology 29:521-524, 1937 24. Stevenson EO, Ozeran RS: Retroperi1934 11. Meyers MA, Evans JA: Effects of pan- toneal space abscesses. Surg Gynecol Obstet creatitis on the small bowel and colon: spread 128:1202-1208, 1969 25. Toxopeus MD, Lucas CE. Krabbenhoft along fascial planes. Am J Roentgen01 (in press) 12. Meyers MA, Whalen JP, Peelle K, et al: KL: Roentgenographic diagnosis in blunt Radiologic features of extraperitoneal effusions: retroperitoneal duodenal rupture. Am J Roentan anatomic approach. Radiology 104:249-257, genol 115:281-288, 1972 26. Welin S: Uber die Rontgenodiagnostik 1972 der Paranephritis. Fortschr Roentgenstr 67:162, 13. Mitchell GAG: The spread of retro1943 peritoneal effusions arising in the renal regions. 27. Wulsin JH: Peptic ulcer of the posterior Br Med J 2:1134, 1939 14. Mitchell GAG: The renal fascia. Br J wall of the stomach and duodenum with retroperitoneal leak. Surg Gynecol Obstet 134: Surg 37:257, 1950 15. Nagamatsu GR: Nontuberculous infec- 425429, 1972