Acute renal and perirenal infections

Acute Renal

and Perirenal

Infections

By JOHN A. EVANS, M.D., MORTON A. MEYERS, M.D., AND MORTON A. BOSNIAK, M.D.

CUTE PYELONEPHRITIS is a common disease,particularly in the female. It occurs most often in childhood and during pregnancy. The classical symptomatology is that of an acute onset with chills, fever, lumbar tenderness and pain, together with dysuria and frequency. Hematuria, macroscopic or microscopic, may be present and renal function may be temporarily abnormal. There are, however, a significant number of patients who have no upper urinary tract symptoms. Acute pyelonephritis may occur either with or without a definitely proved obstructive lesion. It has been known for a long time that infection of the kidney is more frequent when urinary tract obstruction is present. The cases without obstruction have been referred to as primary or uncomplicated pyelonephritis and it is said that many of these heal completely.

A

Pathogenesis and Pathology The kidney becomes infected by one of three routes: via the bloodstream; from the bladder via the ureter (vesicoureteral reflux is the most common cause in childhood) ; and lymphatic spread along the ureter. Heptinstall stated that acute pyelonephritis seen at autopsy is usually severe and associated with obstruction .I6 He noted that there is little pathologic documentation of milder forms of the disease. In the past, this was called pyelitis and it was assumedthe infection was restricted to the renal pelvis. Involvement of the parenchyma in such casesis still debatable. At autopsy the kidney in acute pyelonephritis is usually enlarged because of inflammatory edema. Small abscessesmay be seen on the subcapsular surface. An interesting feature is that significant areas of parenchyma may show no inflammation. Heptinstall said that the sequence of changes from the onset of infection is uncertain. Most investigations have been done in laboratory animals using bloodborne methods of infection along with ureteral obstruction or renal trauma. In the human, although the route of invasion may be bloodborne, it is often an ascending infection that results in pyelitis with spread to the underlying interstitial tissue. Roentgen Appearance There is widespread belief that few if any radiographic abnormalities are seen in acute pyelonephritis. Certainly there is a paucity of descriptive as well

]OHN A. Center, New Hospital-Cornell of Radiology, 274

EVANS, M.D.: York, N.Y. Medical New York

Department of Radiology, New York Hospital-Cornell MORTON A. MEYERS, M.D.: Department of Radiology, Center, New York, N.Y. MORTON A. BOSNIAK, M.D.: Uniuersity Medical Center, New York, N.Y. SEMINARS

IN ROENTGEXOLOGY,

Medical New York Department

VOL. 6, No. 3 (JULY),

1971

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Fig. L-Case 1. Acute cortical abscess in midportion left kidney, proved surgically. This 25-yr-old white woman injured her back 3 wk earlier. Pain in the left flank gradually grew worse and was accompanied by chills and fever. A. Urogram reveals diminished function on the left and persistent spasm of the calices, renal pelvis, and proximal ureter. B. Retrograde examination delineates calices, pelves, and ureters. C. Arteriogram shows displacement of interlobar branches (arrows) about an avascular mass. No abnormal vessels are present. D. Nephrotomogram demonstrates a mass (arrow) in the midportion of the left kidney with an irregular radiolucent center.

Fig. B.-Case 2. Large acute cortical abscess on anterior surface of the left kidney, proved at operation. A 17-yr-old girl with variable but persistent left flank pain accompanied by daily afternoon fever. A. Urogram demonstrates spasm of all left caliceal elements and impaired function. B. Nephrotomogram. Poorly defined, partially radiolucent mass in midportion of left kidney (arrows). C. Arteriogram showing displacement of vessels about an avascular mass. No evidence of abnormal vessels.

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as pictorial material on the urographic changes. Emmett did not deal with acute pyelonephritis as a specific urographic entity.13 Sussman et al. stated that the early changes of pyelonephritis are those of disturbed physiology rather than gross anatomic deformity .Qs This was illustrated by a urogram showing persistent caliceal spasm, Shopfner also referred to impaired ureteral peristalsis during attacks of acute infection. 31 He stated that segmental ureteral dilatation, retention, and reverse peristalsis occur, much like intestinal ileus, and can be observed fluoroscopically. In a group of patients with nonobstructive, acute urinary tract infection studied by Shopfner, the only abnormality in about 15% was dilatation of the ureteropelvic junction comparable to that seen in ureteropelvic obstruction. Except for these studies in infants and children, little investigative effort or interest has been shown in the radiography of the kidneys in acute pyelonephritis. Caliceal deformities are a reflection of disturbed sphincteric activity and may involve one or more caliceal components (Figs. 1 and 2). Dilatation, clubbing, or spasm of calices may be present during the acute phase with reversion to normal after adequate treatment. Inflammatory edema in acute pyelonephritis may cause renal enlargement as well as impaired function (Figs. 3 and 4). RENAL

ABSCESS

Over the past decade there has been considerable improvement in the accuracy of the radiologic diagnosis of various renal diseases. This has been particularly true in the evaluation of neoplasms, cysts, pseudotumors, and vascular disease. The increased diagnostic accuracy has been due mainly to the use of angiography and nephrotomography. However, this precision does not apply to the diagnosis of renal abscess. Renal abscess remains an extremely difficult lesion to recognize preoperatively because the angiographic and nephrotomographic findings are not specific and can mimic benign and malignant renal tumors. The roentgen appearance of renal abscess and necrotic hypemephroma may be identical in every way and only the clinical findings may suggest the diagnosis of abscess.4,7~s,11~17~2s~2Q~s5 Unfortunately, the clinical presentation of renal abscess is usually vague and rarely localizing, and the urine is often negative, so that the diagnosis is frequently missed by the clinician as well. In the great majority of over 200 renal abscesses reported in the literature, the correct diagnosis was not considered preoperatively despite the detection of a mass on intravenous urography. 1Q,27 Yet the differentiation of renal abscess from other conditions is of utmost importance since early correct therapy is essential. A review of the roentgen features of renal abscess is therefore useful. There is a wide spectrum of acute infections of the renal parenchyma ranging from acute pyelonephritis with multiple microscopic cortical abscesses to massive solitary cortical abscess (carbuncle). Perinephritis and perinephric abscess are frequently associated with renal abscess and are part of the overall spectrum of renal inflammatory disease. Perinephric abscess is covered separately, and will be included here only as necessary for completeness.

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Fig. 3.-Case matory edema

EVANS,

3. Inflam-

in a 75 yr-old hypertensive diabetic woman with fever, back pain, pyuria, and mental confusion. A. Urogram reveals large swollen kidneys. Function is severely impaired with only a faint nephrogram. B. Right retrograde pyelogram demonstrates anatomically normal calices, pelvis, and ureter. C. She died 1 mo later. Pathologic specimen shows innumerable, small miliary-like abscesses(arrowheads) scattered throughout parenchyma.

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Fig. 4.-Renal abscess with extension into perirenal tissues. A 64-vr-old man with anemia and weakness. IVP revealed a mass in the left kidney. Left nephrotomogram reveals a large, thick walled, radiolucent mass in the upper pole. The thick wall (arrows) rules out a simple cyst but does not exclude necrotic neoplasm. Confirmed autopsy.

a at

Pathogenesis Renal abscesshas classically been attributed to bloodstream invasion of an infection from another focus in the body. Staphylococcus has been the most common causative organism. However, recent reports indicate that gram negative organisms now predominate, presumably because of earlier, more adequate treatment of the primary staphyloccocal infection with antibiotics.r4*22,30 Another etiologic factor emerging during the past few years is drug addiction with “mainlining.” Renal abscessmay also be secondary to suppurative pyelonephritis ascending via the lymphatics. This is usually due to a coliform bacil1uss7 and is frequently associated with calculus disease or urinary tract obstruction. Classically, infected emboli lodge in the small arteries of the kidney. The bacteria multiply and the infected foci enlarge with formation of multiple small abscesses.These may then coalesce to form a single large, sometimes multiloculated abscess often referred to as a renal caTbuncb.l~14~22~2’,30The lesion is parenchymal and has no communication with the collecting system; hence no pus is found in the urine. After the abseessforms, there are three pathways of extension: through the renal capsule, causing a perinephritis or perinephric abscess; into the renal pelvis, resulting in drainage and cavitation; and continued enlargement and progression within the parenchyma, to become a larger and more chronic inflammatory mass.12

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Clinical Presentation Evaluation of a large series of renal abscesses indicates that the condition is most common in the young adult but it has been reported in all age groups, from newborns to the elderly, more frequently in males. It is usually unilateral and somewhat more common on the right.11 12,14~si~2a~27~sa Apparently two different clinical pictures of renal abscess are seen, the acute and the chronic. In the acute episode, fever, chills, malaise, and leukocytosis occur. Sometimes there are pain and tenderness localized to the flank. A history of recent infection or trauma (the injured kidney is more susceptible to infection) is helpful. Urinary symptoms are usually absent and urinalysis is usually not of diagnostic aid. Localizing signs can lead to a diagnosis of possible renal abscess on clinical grounds. In those patients whose symptoms develop more slowly and reach a subacute or chronic status without being detected in the acute phase, the diagnosis becomes much more difficult. This course may be attributable to antibiotic treatment which allows a more chronic condition to develop while controlling the acute phase of the disease. In the chronic phase, the clinical picture of sepsis is not as clearly defined and the fever and leukocytosis are not as marked. Also, localizing signs such as flank pain, guarding, and tenderness are rare. Urinary tract symptoms are not prominent and urinalysis is usually negative.1~g~14~21~ss~saThe presentation may simulate that of a renal neoplasm. No wonder the correct preoperative diagnosis of renal carbuncle has been made in less than 20% of reported cases.12 Emmett believes that the problem of diagnosis is chiefly clinical rather than radiologic and states that, “If one waits for gross urographic changes to occur before making a diagnosis, valuable time may be lost.“13 Actually, though, it is really not possible to make a definitive diagnosis of renal abscess without radiologic help, as radiography can confirm the presence of a renal mass and will also rule out obstruction (pyonephrosis) which might give a similar clinical picture. Roentgen Appearance The radiologic findings in acute parenchymal infection depend on the stage (acute, subacute, or chronic) of the abscess and the type of extension that has occurred. In the acute phase, intravenous urography will usually show a variable degree of decreased opacification of the entire kidney or a portion of it. If there are multiple small renal abscesses, the kidney may appear enlarged and swollen with little or no opacification, similar to severe acute pyelonephritis (Fig. 3A). When the infection is localized as a single large abscess, a bulge in the outline of the kidney may be detectable. Caliceal distortion will also be seen if the mass is large enough. If extension into the perirenal space has occurred, loss of sharp renal outline and of mobility of the kidney on respiration will occur. Caliceal destruction and cavitation will be seen if the abscess has extended into the collecting system. This does not happen frequently, but when present, simplifies the diagnosis.13, 1s Retrograde pyelography usually is not indicated unless visualization of the

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collecting system is poor or absent on urography or unless caliceal irregularity or cavitation is seen. A condition that must be differentiated is acute pyonephrosis. If the kidney is nonfunctioning, a retrograde pyelogram is indicated to rule out obstruction. Nephrotomography will confirm the urographic findings. In the acute stage, the abscess may appear as a poorly demarcated, lucent defect in the kidney ( Fig. 2B ) . The findings may simulate a benign cyst but the margins of the mass are not as sharp and, if the mass extends to the surface of the kidney, its wall will appear thicker than a simple cyst. The more chronic the abscess, the thicker will be its capsule and the more irregular its margins. In the subacute and chronic phases the lesion will have all of the nephrotomographic characteristics of a necrotic neoplasm10 (Fig. 4). Nephrotomography aids in defining the mass and the renal margins more clearly, thereby demonstrating perirenal extension. Nephrotomography’s role, then, is to confirm the urographic findings, show that the lesion is not a benign cyst, and indicate when angiography should be performed. Arteriography outlines the renal abscess most successfully. The findings will depend, of course, on the stage of the abscess and its extent. In acute abscess, the major roentgen finding is displacement of vessels about a mass. There is a diminished nephrogram and loss of the usual sharp renal margin at the site of the lesion. No abnormal or tumor vessels will be seen (Figs. 1D and 2C). A slight increased blush may be noted at the margin of the lesion which is due both to compression of surrounding parenchyma and to increased vascularity at the margin of the lesion.16 The lesion at this stage could be confused angiographically with a cyst except that its margins are not sharp but rather indistinct and hazy. These findings are hardly specific and can also be seen in a poorly vascularized neoplasm or granuloma. However, as described earlier, at this stage the patient may present clinically with acute flank pain, high fever, and leukocytosis arousing suspicion of renal abscess. In such instances, the radiologist can confirm the presence of an avascular mass and suggest the diagnosis of a renal abscess. This is of great help to the surgeon, who will then know the size and extent of the abscess preoperatively and possibly be able to avoid nephrectomy by merely incising and draining the abscess. Angiographically, the appearance of chronic abscess is identical to that of a poorly vascularized renal cell carcinoma.4,7~s,rr,ra, rs~17~25~2s,a1~33,35In this respect, it differs from the usually avascular acute abscess. The kidney has had more time to react to the inflammatory changes so that the capsule is thicker and vascularity is increased, particularly along the margins of the lesion. Abnormal vessels indistinguishable from so-called tumor vessels are present (Fig. 5). These inflammatory vessels represent arteries that have hypertrophied to feed the inflammatory mass and are tortuous and irregular. A dense blush is seen during the capillary-nephrogram phase. Even early venous filling has been seen in some cases of renal abscess .ll If the abscess extends into the perirenal space, vessels (perforating capsular arteries) from the kidney supply the infected area (Fig. 6). Hypertrophy of capsular arteries also occurs. It was hoped that the use of epinephrine angiography would help differen-

EVANS,MEYERS,ANDBOSNIAK

Fig. 5.-Chronic abscess. A 63-yr-old woman with 3-mo history of low-grade fever and flank pain. IVP revealed a mass at the upper pole of the left kidney. The renal arteriogram demonstrates the mass to be hypovascular although some abnormal vessels (arrow) extend into it from the adjacent parentihyma. The appearance is identical to that of a hypovascular neoplasm. At operation, a chronic abscess of the upper

pole with extension into the perirenal

space was found.

tiate abscessfrom necrotic hypernephroma. Theoretically, the use of epinephrine should constrict the vessels to an abscessbut should not affect tumor vessels. Unfortunately this has not been the case. In two published reports and in our own experience, the use of epinephrine-enhanced angiography was not diagnostically helpful .spr7 In renal abscess,a positive epinephrine test was obtained (i.e., the inflammatory vessels behaved as tumor vessels). Kahn believes that this might be dose related and appropriate dosage of epinephrine may aid in this distinction.17 Therefore, at present a specific diagnosis of chronic renal abscesscannot be made purely on radiographic evidence. As in other organs, angiography is unable to differentiate betwen infection and neoplasm, so that renal abscess should always be considered in all cases diagnosed as hypovascular renal neoplasm. Luckily, abscessis comparatively rare when compared with renal cell carcinoma and the treatment for far advanced renal abscessis probably the same as for renal malignancy. PEIURENAL

Anatomic

ABSCESS

Con&kration.s

Knowledge of the fascial relations and attachments of the kidney (Fig. 7) is essential to an understanding of the development and spread of perirenal infection. The renal fascia is a collagenous, elastic connective tissue sheath of

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Fig. 6.-Chronic ing into perirenal

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renal abscess extendspace. Angiogram re-

veals many abnormal vessels(perforating and capsular) penetrating the perirenal mass. medium or dense consistency that invests the kidneys and adrenal gland fairly closely. Between the renal capsule and its fascial envelope lies a variable amount of perirenal fat which is most abundant posteriorly and laterally. This fatty space is traversed by septa and connecting blood vessels and lymphatics. The lines of fusion of the anterior and posterior renal fascial planes tend to direct the dissection of exudate within this retroperitoneal compartment. Superiorly the two layers are firmly fixed to each other above the adrenal glands to the diaphragmatic fascia. Laterally, beyond the most abundant portion of the perirenal fat, they fuse to form the lateroconal fascia.lO This relates

to the posterior

aspect

of the

colon

and

terminates

by uniting

with

the connective tissue layer of the peritoneal reflection which forms the paracolic gutter. Deep to the posterior renal fascia and anterior to the tranversalis fascia lies another variable fat deposit, the pararenal fat, which is contiguous with

the extraperitoneal fat seen in the flank stripe. Fig. 7.-Fascial relations of kidney. Transverse section (viewed from above) at level of L2. RK: right kidney; LK: left kidney; A: aorta; WC: inferior vena cava; SMA and SMV: superior mesenteric artery and vein; P: pancreas; DD: descending duodenum; DC: descendPM: psoas colon; % major; QL: quadratus muscle; 1: posterior parietal peritoneum; 2: anterior lumborum renal fascia; 3: extraperitoneal flank fat stripe; 4: lateroconal fascia; 5: perirenal fat; 6: posterior renal fascia; 7: pararenal fat; 8: transversalis fascia.

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Originally, Gerota claimed bilateral continuity of the perirenal compartments deep to the anterior renal fasciae. 1s However, subsequent precise dissections and injection experiments have shown that the two perirenal spaces are neither in actual nor potential direct communication. Medially, the posterior fascial layer fuses with the psoas or quadratus lumborum fascia, and the anterior renal fascia blends in the dense mass of connective tissue surrounding the great vessels in the root of the mesentery and behind the pancreas and duodenum.lQ,QQ Where the kidneys are in contact with the pancreas, duodenum, and colon, the anterior renal fascia becomes less distinguishable as a fascial plane and blends with the intervening layers of connective tissue. The extraperitoneal space enclosed by the renal fasciae narrows as it extends inferiorly and medially so that it has been likened to an inverted cone.10 Inferiorly, the layers fuse weakly or blend with the iliac fascia; as they narrow medially, they also blend loosely with the periureteric connective tissue. Mitchell has shown that the weakest point, through which perirenal effusions escape most easily, is at the inferomedial angle of the perinephric space adjacent to the ureter. 19 At this level, spread may occur across the midline to the opposite side or into the pelvis. With greatly increased pressure in the perirenal space, transperitoneal rupture may occur in the region of the renal hilus.26 Pathogenesis It has become increasingly apparent that most cases of perirenal abscess in the adult are secondary to a focus of renal infection.26 A renal cortical abscess or carbuncle, perhaps associated with pyonephrosis, may perforate the capsule and contaminate the perirenal space. Perforation of the ureter or a caliceal fornix (e.g., by instrumentation or back pressure from an obstructing calculus) with discharge of infected urine may lead to a smoldering perirenal abscess. At times, the underlying site of renal communication is difficult to identify, even at operation. Some have thought that the rich vascular and lymphatic connections of the renal parenchyma with the perirenal fat provide the pathway for the spread. The offending organism is usually E. coli., B. proteus, or a streptococcus. Bilateral involvement is rare and is secondary to bilateral renal infections.32 Spread to the perirenal space from adjacent extraperitoneal sites of infection may occur, as from diverticulitis, perforated carcinoma of the colon, retroperitoneal appendicitis, pancreatitis, or pelvic inflammatory conditions. Inflammatory spondylitis is also included in this group, although it more commonly leads to an extrafascial abscess. Hematogenous spread from remote sites of infection, such as furunculosis, wound infection, or upper respiratory disease also occurs.2~34 This is more common in children; the offending organism is usually Staphylococcus aureus. Clinical

Considerations

Acute infection of the perirenal space is marked by fever, chills, flank pain, a tender bulging flank, and leukocytosis. The cause in the adult is generally quite

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evident. The clinical course of perirenal abscess, on the other hand, is usually insidious and chronic. Recognition of the process is frequently difficult and delayed.26 Malaise, weight loss, and low grade fever may be present for weeks to months before localizing signs develop. A mass is palpable only if large or if it localizes inferiorly below the costal margin. With pressure on the extraperitoneal nerves, pain may be referred to the groin, thigh, or knee.16 If the condition is suspected clinically, roentgen confirmation is relied upon. It is noteworthy that of 17 cases of perirenal abscess diagnosed roentgenographically by Welin, the clinical diagnosis had not been considered in eight.36 Roentgen

Findings

These are closely related to the severity and extent of the inflammatory process. A diffuse infection of the perirenal space presents differently from a localized abscess. The associated underlying primary renal disease itself may alter the urographic changes. In view of the varying clinical signs of perirenal inflammatory disease, rigid adherence to relating the roentgen alteration to the presumed onset of the process may be misleading.28 Negative radiographic findings practically exclude the possibility of chronic perirenal abscess. In acute perinephritis or perirenal abscess, however, the roentgen findings may be uncertain initially, so that repeated examinations may be necessary to make the diagnosis.28 As a rule, a single roentgen finding is nonspecific because it may be due to some other disease. But in combination, the roentgen signs usually permit the correct diagnosis. For purposes of practical application, they may be grouped into primary and secondary radiologic signs. Primary roentgen signs include: (1) Loss of renal outline with increased density in region of kidney. (2) Displacement of the kidney. (3) Axial rotation of kidney. Perirenal infection may be either diffuse and poorly defined or in the form of a localized mass. Loss of a segment of the perirenal fatty contrast may indicate the site of the process. The exudate usually localizes in the rich dorsolateral perirenal fat near the lower pole because the infection follows the path of least resistance, abetted by gravity in the supine position, The kidney is therefore usually displaced medially and upward and may be rotated about its vertical axis (Figs. 8 and 9). On frontal supine films, the affected kidney may appear larger because of magnification; a lateral film will then document its anterior displacement. The suspected side should be dependent for the lateral view since in this position the normally located kidney does not project anterior to the lumbar spine. Loculations in other parts of the perirenal space may produce renal displacement and rotation in other axes. As the exudate increases, it tends to seek the infrahilar area, extending inferiorly along the ureter. Loss of definition with lateral displacement of the inferior renal pole will then result. (4) Extrinsic compression of the renal pelvis and proximal ureter. The mass tends to press from the lateral aspect so that the proximal ureter may also be

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Fig. 8.-Right perirenal abscess. The collection in the dorsolateral fat near the lower pole displaces the kidney u ward and medially, deflects the upper ureter medially, and obscuresthe proximaf psoasmargin. Note the loss of contrast of the perirenal fat and renal outline.

displaced anteriorly over the psoas muscle as well as medially. Compression may be severe enough to cause dilatation of the upper collecting system. (5) Fixation of the kidney. Normally, renal mobility of 2 to 6 cm can be shown on erect views or with respiratory excursions.3 A perinephric process tends to fix the kidney in the majority of patients.2s (6) Extravasation into perirenal space. Communication of the collecting system with the perirenal compartment is presumptive evidence of a perirenal abscess in all but the most acute circumstances. The extravasation may be demonstrated by retrograde pyelography or fistulography ( Fig. 10). (7) Perirenal gas. Gas producing infection secondary to E. CO&, Aerobacter aerogenes, or, rarely, Clostridiu, occurs, especially among diabetics. The gas may encircle the kidney or present as a mottled localized collection of radiolucencies within the shadows of the perirenal fat (Fig. 11). Fluid levels may be identified in the upright position.6

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Fig. 9.-Perirenal abscess. Retrograde pyelogram shows characteristic upward and medial displacement of the kidney and proximal ureter with axial rotation of the kidney by a large mass which also displaces the hepatic flexure of the colon downward. There is loss of visualization of the renal outline and psoas margin.

(8) Displacement of contiguous bowel. A collection of pus in the perirenal compartment may produce a masseffect upon adjacent intestine. On the right, the descending duodenum may be displaced medially and anteriorly and the hepatic flexure of the colon downward. On the left, the distal transverse colon

Fig. lO.-Perirenal abscessafter pyelolithotomy with stenosis at the ureteropelvic junction. Injection through a nephrostomy tube shows gross extravasation into the perirenal compartment.

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Fig. Il.-Gas producing perirenal infection in a diabetic woman. Multiple radiolucencies throughout the enlarged left perirenal compartment. Note the prolonged nephrogram secondary to shock.

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Fig. 12.-Massive perinephric abscess secondary to calculus pyonephrosis. Plain film shows

increased density, loss of kidnev outline, and numerous ‘renal calculi. The abscesshas dis laced the transverse and f;escending colon. (Courtesy of Dr. G. R. Nagamatsu; reproduced with permissionof the publisher.23)

may be displaced superiorly or inferiorly, and the duodenojejunal junction medially (Fig. 12). (9) Arteriographic findings. Arteriography may be of particular value in cases where the conventional radiographic findings are uncertain or where primary renal infection is suspected to extend through the capsule. The angiogram may define the size and location of the abscess.Characteristically, the findings include increased number and size of the perforating arteries extending from the kidney, stretching of tortuous and prominent capsular and perhaps pelvic arteries around the abscess margin, and a contrast blush’ (Fig. 6). Seconday roentgen signs include: ( 1) Absence of a segment of the psoas muscle margin. If the process extends medially and inferiorly along the ureter, the water density of the exudate and associated edema may obscure the fatty contrast along the muscle border. Localized asymmetry of the psoas shadow in properly centered films is the most dependable way to avoid a false-positive sign. The extraperitoneal fat may be scanty, especially in patients with emaciation or weight loss. The psoas outline may also disappear with very slight rotation of the lumbar spine or with scoliosis.32 (2) Scoliosis. This occurs in less than half the patients with perinephric abscess.28

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(3) Restriction of diaphragmatic motility and pulmonary basilar changes. Nesbit and Dick showed that of 85 patients with perirenal abscesses,14 (16.5%) had supraphrenic complications. 24 This may vary from a minimal pleuritis to effusion, pneumonia, and nephrobronchial fistula. Excursion of the ipsilateral hemidiaphragm, especially its posterior segment, may be restricted or absent. (4) Infiltration of flank stripe. Blurring and widening of the extraperitoneal flank fat indicate widespread extension into the pananephric tissues.32

REFERENCES 1. Anderson, W. A. D. (Ed.) : Pathology. St. Louis, Mosby, 1948. 2. Atcheson, D. W.: Perinephric abscess with a review of 117 cases. J. Urol. 46201, 1941. 3. Bacon, R. D.: Respiratory pyelography: a study of renal motion in health and disease. Amer. J. Roentgen. 44:71, 1940. 4. Becker, J. A., Fleming, R., Kanter, I., and Melicow, M.: Misleading appearances in renal angiography. Radiology 88691, 1967. 5. Bosniak, M. A., and Faegenburg, D.: The thick-wall sign: an important finding in nephrotomography. Radiology 84:692, 1965. 6. Braman, R., and CTOSS, R. R., Jr.: Perinephric abscess producing a pneumonephrogram. J. Urol. 75:194, 1956. 7. Caplan, L. H., Siegelman, S. S., and Bosniak, M. A.: Angiography in inflammatory space-occupying lesions of the kidney. Radiology 88:14, 1967. 8. Caro, G., Meisell, R., and Held, B.: Epinephrine-enhanced arteriography in renal and perirenal abscess: a differential diagnostic problem. Radiology 92: 1262, 1969. 9. Cobb, 0. E.: Carbuncle of the kidney. Brit. J. Urol. 38:262, 1966. 10. Congdon, E. D., and Edson, J. N.: The cone of renal fascia in the adult white male. Anat. Rec. 80:289, 1941. 11. Combs, J. A, Crummy, A. B., and Cossman, F. P.: Angiography in renal and pararenal inflammatory lesions: the significance of early venous filling. Radiology 98:401, 1971. 12. Doolittle, K. H., and Taylor, J. N.: Renal abscess in the differential diagnosis of mass in kidney. J. Urol. 89:649, 1963. 13. Emmett, J. L.: Clinical Urography (ed. 2). Philadelphia, Saunders, 1964.

14. Fair, W. R., and Higgins, M. H.: Renal abscess. J. Urol. 104:179, 1970. 15. Gerota, D.: Beitrage zur Kenntniss des Befestigungsapparates der Niere. Arch. Anat. Entwckhrgsgesch. pp. 265-285, 1895. 16. Heptinstall, R. H.: Pathology of the Kidney. Boston, Little, Brown, 1966, p. 402. 17. Kahn, P. C., and Wise, H. M., Jr.: Simulation of renal tumor response to epinephrine by inflammatory disease. Radiology 89: 1062, 1967. 18. LeComte, R. M.: Perinephritis and perirenal abscess. J. Urol. 56:636, 1946. 19. Mitchell, G. A. G.: The spread of retroperitoneal effusions arising in the renal regions. Brit. Med. J. 2:1134, 1939. 20. -: The renal fascia. Brit. J. Surg. 37: 257, 1950. 21. Moore, C. A., and Gangai, M. P.: Renal cortical abscess. J. Urol. 98:303. 1967. 22. Murphy, J. J., and Kohler, F. P.: Reevaluation of modem antibacterial agents used for perirenal abscess. JAMA 171:1287, 1959. 23. Nagamatsu, G. R.: Nontuberculous infections of the kidney. In Ney, C., and Friedenberg, R. M. (Eds. ) : Radiographic Atlas of the Genitourinary System. Philadelphia, Lippincott, 1966, p. 110. 24. Nesbit, R. M., and Dick, V. S.: Pulmonary complications of acute renal and perirenal suppuration. Amer. J. Roentgen. 44: 161, 1940. 25. Olsson, O., and Jiinsson, G.: Roentgen examination of the kidney and ureter. In Alken, C. E. et al. (Eds.) : Encyclopedia of Urology, Vol. V. Radiology. I. Diagnostic Radiology. Berlin, Springer-Verlag, 1962. 26. Parks, R. E.: The radiographic diagnosis of perinephric abscess. J. Urol. 64:555, 1950.

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