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All the key Radiology cases for your rounds, rotations, and exams - in print and online!
Genitourinary Imaging will enable you to diagnose the full range of cases involving the genitourinary system.
Features of Genitourinary Imaging:
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Veröffentlichungsjahr: 2011
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Edited by
Shailendra Chopra, MD, MRCP, FRCR
Section HeadDepartment of RadiologyLexington ClinicVoluntary Associate Professor of RadiologyUniversity of KentuckyLexington, Kentucky
Series Editors
Jonathan Lorenz, MD
Associate Professor of RadiologyDepartment of RadiologyThe University of ChicagoChicago, Illinois
Hector Ferral, MD
Professor of RadiologySection Chief, Interventional RadiologyRUSH University Medical Center, ChicagoChicago, Illinois
ThiemeNew York • Stuttgart
Thieme Medical Publishers, Inc.333 Seventh Ave.New York, NY 10001
Executive Editor: Timothy HiscockEditorial Assistants: Michael Rowley and Adriana di GiorgioEditorial Director, Clinical Reference: Michael WachingerProduction Editor: Katy Whipple, Maryland CompositionInternational Production Director: Andreas SchabertVice President, International Marketing and Sales: Cornelia SchulzeVice President, Finance and Accounts: Sarah VanderbiltPresident: Brian D. ScanlanCompositor: MPS Limited, a Macmillan CompanyPrinter: Sheridan
Library of Congress Cataloging-in-Publication Data
Genitourinary imaging / edited by Shailendra Chopra. p. ; cm.—(RadCases) Includes bibliographical references. ISBN 978-1-60406-324-01. Genitourinary organs—Imaging—Case studies. I. Chopra, Shailendra. II. Series: RadCases. [DNLM: 1. Urography—Case Reports. 2. Diagnosis, Differential—Case Reports.3. Diagnostic Imaging—Case Reports. 4. Female Urogenital Diseases—radiography—Case Reports.5. Male Urogenital Diseases—radiography—Case Reports.WJ 141] RC874.G44 2011 616.6′07572—dc23
2011019982
Copyright © 2012 by Thieme Medical Publishers, Inc. This book, including all parts thereof, is legally protected by copyright. Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation without the publisher's consent is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing or duplication of any kind, translating, preparation of microfilms, and electronic data processing and storage.
Important note: Medical knowledge is ever-changing. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may be required. The authors and editors of the material herein have consulted sources believed to be reliable in their efforts to provide information that is complete and in accord with the standards accepted at the time of publication. However, in view of the possibility of human error by the authors, editors, or publisher of the work herein or changes in medical knowledge, neither the authors, editors, nor publisher, nor any other party who has been involved in the preparation of this work, warrants that the information contained herein is in every respect accurate or complete, and they are not responsible for any errors or omissions or for the results obtained from use of such information. Readers are encouraged to confirm the information contained herein with other sources. For example, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this publication is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs.
Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain.
Printed in the United States of America
978-1-60406-324-0
Dedication
To my wife Kathy, whose love and support make my endeavors possible, and to my daughter Nicky, whose hope in the future makes them worthwhile.
RadCases Series Preface
The ability to assimilate detailed information across the entire spectrum of radiology is the Holy Grail sought by those preparing for the American Board of Radiology examination. As enthusiastic partners in the Thieme RadCases Series who formerly took the examination, we understand the exhaustion and frustration shared by residents and the families of residents engaged in this quest. It has been our observation that despite ongoing efforts to improve Web-based interactive databases, residents still find themselves searching for material they can review while preparing for the radiology board examinations and remain frustrated by the fact that only a few printed guidebooks are available, which are limited in both format and image quality. Perhaps their greatest source of frustration is the inability to easily locate groups of cases across all subspecialties of radiology that are organized and tailored for their immediate study needs. Imagine being able to immediately access groups of high-quality cases to arrange study sessions, quickly extract and master information, and prepare for theme-based radiology conferences. Our goal in creating the RadCases Series was to combine the popularity and portability of printed books with the adaptability, exceptional quality, and interactive features of an electronic case-based format.
The intent of the printed book is to encourage repeated priming in the use of critical information by providing a portable group of exceptional core cases that the resident can master. The best way to determine the format for these cases was to ask residents from around the country to weigh in. Overwhelmingly, the residents said that they would prefer a concise, point-by-point presentation of the Essential Facts of each case in an easy-to-read, bulleted format. This approach is easy on exhausted eyes and provides a quick review of Pearls and Pitfalls as information is absorbed during repeated study sessions. We worked hard to choose cases that could be presented well in this format, recognizing the limitations inherent in reproducing high-quality images in print. Unlike the authors of other case-based radiology review books, we removed the guesswork by providing clear annotations and descriptions for all images. In our opinion, there is nothing worse than being unable to locate a subtle finding on a poorly reproduced image even after one knows the final diagnosis.
The electronic cases expand on the printed book and provide a comprehensive review of the entire subspecialty. Thousands of cases are strategically designed to increase the resident's knowledge by providing exposure to additional case examples—from basic to advanced—and by exploring “Aunt Minnie's,” unusual diagnoses, and variability within a single diagnosis. The search engine gives the resident a fighting chance to find the Holy Grail by creating individualized, daily study lists that are not limited by factors such as a radiology subsection. For example, tailor today's study list to cases involving tuberculosis and include cases in every subspecialty and every system of the body. Or study only thoracic cases, including those with links to cardiology, nuclear medicine, and pediatrics. Or study only musculoskeletal cases. The choice is yours.
As enthusiastic partners in this project, we started small and, with the encouragement, talent, and guidance of Tim Hiscock at Thieme, continued to raise the bar in our effort to assist residents in tackling the daunting task of assimilating massive amounts of information. We are passionate about continuing this journey, hoping to expand the cases in our electronic series, adapt cases based on direct feedback from residents, and increase the features intended for board review and self-assessment. As the American Board of Radiology converts its certifying examinations to an electronic format, our series will be the one best suited to meet the needs of the next generation of overworked and exhausted residents in radiology.
Jonathan Lorenz, MDHector Ferral, MDChicago, IL
Preface
Acquiring knowledge of the imaging presentations of different diseases and knowing the differential diagnoses of various findings is a part of the evolution of the budding radiologist. But being able to apply that knowledge to actually deal with a million or so cases that you as a radiologist will see in a lifetime of practice is the pinnacle of your training. Some of those cases will be a part of the board examination, which is an exaggerated cross-section of your daily practice. This book is written with the confidence that it will give you the tools and examples of how to apply that knowledge whether in the examination setting or in real life.
The cases in this book are all from the daily practice of genitourinary (GU) imaging. I assure you, none of them have been invented. The book and its companion web-based section contain cases that are the common presentations of various GU disease entities. There are potentially fatal conditions that need to be diagnosed to avert disaster, and there are benign conditions that need to be recognized as such to avoid subjecting the patient to unnecessary and potentially dangerous further investigation. The cases are not arranged in any particular order, but picking up any 10 cases in order will give you a sample of the entire breadth of GU imaging similar to what you can expect to see on the exam.
Finally, our training as radiologists does not end with passing the boards. We must learn throughout our professional lives to maintain that edge of proficiency. Two processes are particularly helpful in doing that. One is talking to your clinical referring colleagues regularly about their practice and their expectations, because it is through them that we serve our patients. Second is to follow up your cases and learn from the incorrect as well as correct diagnoses that you make. The material in this series will help you not only in passing the boards but also in supplementing your learning long after you have achieved that success.
Acknowledgments
I would like to thank Hector Ferral, MD, for inviting me to be a part of this excellent series; Rajeev Suri, MD (University of Texas Health Science Center, San Antonio, Texas) and Cynthia M. Day, MD (Brigham and Women's Hospital, Boston, Massachusetts), for allowing me to use some of their cases; and Timothy Hiscock and his team at Thieme for their insightful guidance and interminable (almost) patience in the production of this work.
A 62-year-old woman with gross hematuria.
The contrast-enhanced computed tomography (CT) sections through midabdomen show a heterogeneously enhancing mass (arrow) occupying the interpolar region of the left kidney. The mass is centered in the renal parenchyma and causes contour deformity of the kidney. It is not surrounded by a dilated collecting system. No involvement of neighboring structures is seen. No lymphadenopathy is seen in these sections. Left renal (arrowhead) vein is well seen and shows no enlargement or obvious filling defect.
• Renal cell carcinoma (RCC): Heterogeneous enhancement of the mass and origin from the renal parenchyma are findings characteristic of RCC.
• Oncocytoma: This also presents as an enhancing mass arising from the renal parenchyma. A spoke wheel pattern of enhancement is considered characteristic. However, because it cannot be reliably distinguished from RCC and is much less common than that entity, oncocytoma should not be diagnosed prospectively
• Lipid-poor angiomyolipoma: This is a rare entity. Unlike in the typical angiomyolipoma, no fat is seen within the lesion. Enhancement may be present. A preoperative imaging diagnosis is not reliable.
• RCC is the most common solid mass in the kidney. It is more common in males and generally seen in patients older than 40 years. However, it is becoming more common to encounter cases in younger age groups.
• The most common histologic subtype is the clear cell type. The other, less common subtypes are papillary, chromophobe, and sarcomatoid.
• Painless hematuria is the most common presentation. A palpable mass may be present if the tumor is large. Patients may present with a paraneoplastic syndrome. An increasing number of cases are being found incidentally on cross-sectional imaging performed for other indications.
• Spread occurs locally into the perinephric fat or adrenal gland, through lymphatics into the retroperitoneal lymph nodes, and via the vascular route to distant organs like the lungs, bones, liver, brain, or opposite kidney. The frequency of metastases increases with the size of the tumor, and metastasis of tumors < 3 cm is rare. Invasion into the renal vein is seen with large tumors and can be easily demonstrated by contrast-enhanced CT.
• On CT, RCC typically appears as a solid mass with its center located within the renal parenchyma. Large tumors often cause contour deformity of the kidney. Enhancement after intravenous contrast is always present and may vary in intensity depending on tumor vascularity and time elapsed after injection of contrast. Therefore, multiphasic CT with images obtained in the precontrast, corticomedullary, nephrographic, and sometime excretory phases is the optimal protocol to characterize a renal lesion.
• On ultrasound, RCC has solid appearance. Larger lesions are often heterogeneous because of hemorrhage or necrosis. Renal vein extension may be seen by Doppler examination.
• Magnetic resonance imaging shows RCC as a mass with variable signal intensity on T1- and T2-weighted images. Contrast-enhanced dynamic sequences are necessary for the diagnosis and show enhancement to variable degrees in different phases. Subtraction images are critical in the detection of mild parenchymal enhancement.
• Primary lesions of RCC are often not hypermetabolic on positron emission tomography (PET). Metastatic lesions may or may not be hypermetabolic. Therefore, a negative PET exam does not rule out RCC.
In all cases of renal masses, look for perinephric invasion, retroperitoneal lymphadenopathy, renal vein invasion, and obvious metastases in the bones and viscera included in the images.
All enhancing solid renal masses that do not have fat should be considered malignant unless proven otherwise by pathology. Even though some of the enhancing non–fat-containing renal lesions will turn out to be benign oncocytomas or lipid-poor angiomyolipomas, there is no reliable way of diagnosing them on imaging.
A 24-year-old woman with a history of recurrent urinary tract infection since childhood.
(A) Thick-slab multiplanar reconstruction (MPR) image from the excretory phase of a computed tomographic (CT) intravenous pyelogram (IVP) study shows that the right kidney is small. The outline is irregular because of asymmetric parenchymal loss caused by scarring (arrows) overlying dilated upper pole calices (arrowheads). The left kidney is normal. (B) Thick-slab MPR image anterior to the level of Figure A shows scarring (arrows) overlying dilated interpolar and lower pole calices (arrowheads). There is no dilatation of the right renal pelvis (asterisk). The left kidney is normal.
• Reflux nephropathy: This is the most common cause of unilateral or bilateral small, scarred kidneys. Loss of parenchyma occurs characteristically in the regions overlying the calices. The calices are often dilated and may show deformity. The upper pole is more commonly involved.
• Scarring due to multiple old infarcts: This is a much less common cause of unilateral or bilateral small, scarred kidneys. Infarcts may have been associated with previous sickle cell disease or may have resulted from multiple episodes of systemic emboli in the past. Parenchymal loss is seen in between the calices, which may show some crowding but characteristically are not dilated. No polar predilection is present.
• Fetal lobation: This is not uncommon. It is bilateral. There is no parenchymal loss, and the kidneys are normal in size.
• Reflux nephropathy is the most common cause of small, scarred kidneys. It is more common in women.
• Reflux nephropathy is the result of vesicoureteric reflux during childhood. Although infection may have some role in the pathogenesis, the presence of intrarenal reflux is considered more important.
• Scars overlying blunted calices are the hallmark of reflux nephropathy. The scars may occur anywhere in the kidney. However, because the renal poles have compound calices and a less efficient mechanism to prevent intrarenal reflux, the scarring is much more severe at the renal poles, particularly the upper pole. Scarring generally occurs before the age of 4 years.
• Although reflux nephropathy may result in poor renal function if it involves both kidneys, unilateral involvement is asymptomatic. A history of vesicoureteric reflux from childhood may or may not be available.
• Scarring of the kidney due to reflux nephropathy can be recognized on IVP, ultrasound, CT, and magnetic resonance imaging as parenchymal defects filled with perinephric fat. Most cases in adults are detected by CT as an incidental finding. In children, ultrasound and dimercaptosuccinic acid scans are equally accurate in detecting parenchymal scars. When scarring is unilateral in adults, the contralateral kidney may show compensatory hypertrophy. Compensatory hypertrophy also develops in the unaffected portions of the scarred kidney. These normal areas may become large enough to give the appearance of a mass (pseudotumors).
In adults, it is important to recognize a scarred kidney due to reflux nephropathy correctly to avoid unnecessary investigation of the areas of scarring or pseudotumors.
When scarring of the kidneys is detected in children, voiding cystourethrography should be performed to look for vesicoureteric reflux and, if it is present, institute treatment.
A 74-year-old woman with a history of fullness in the right flank.
(A) Longitudinal sonographic image of the right kidney shows complete atrophy of the right renal parenchyma. The right renal pelvis (asterisk) and calices (arrowheads) are dilated. There is also dilatation of the right proximal ureter. (B) Longitudinal sonographic image of the normal left kidney in the same patient shows that the renal parenchyma (arrow) is normal in thickness. The renal sinus fat (asterisk) is normal, and there is no hydronephrosis. The normal, somewhat hypoechoic renal pyramids (arrowheads) should not be mistaken for caliceal dilatation.
• Chronic right hydronephrosis and hydroureter: There is dilatation of the collecting system as well as the ureter. The dilated collecting system appears as a fluid-filled structure with connecting fluid-filled, dilated branches. The severity of dilatation and degree of parenchymal atrophy depend on the duration of obstruction. Usually, it is possible to follow the ureter to the transition point by ultrasound, and computed tomography (CT) is necessary to determine the level and cause of obstruction.
• Right hydronephrosis due to ureteropelvic junction obstruction: This usually manifests in children or young adults, although it may present at a later age. The dilatation and parenchymal atrophy are usually more severe in congenital cases. The ureter is not dilated.
• Parapelvic cyst: This is more common than hydronephrosis. Because these cysts are often multiple, they may closely mimic hydronephrosis on ultrasound. However, the apparent branching structures do not communicate with one another. Nevertheless, sometimes it may be impossible to differentiate them from hydronephrosis without contrast-enhanced excretory phase images.
• When unilateral hydronephrosis is associated with hydroureter, it is always due to obstruction of the ipsilateral ureter or ureterovesical junction (UVJ). Ureteric obstruction can be due to intrinsic causes like stone or blood clot, mural causes like benign stricture or neoplasm, or extrinsic causes like malignant lymphadenopathy or pelvic mass. UVJ obstruction can be due to a stone impacted at the UVJ or to a bladder neoplasm.
• Acute obstruction of the ureter may cause some hydronephrosis but is usually mild and shows no parenchymal atrophy. That is because with acute complete obstruction, the kidney shuts down and no more urine is produced to accumulate in and dilate the collecting system.
• When the obstruction is chronic or partial, the collecting system and ureter dilate up to the point of obstruction. The renal parenchyma begins to atrophy because of back pressure interfering with perfusion. The ureter not only dilates but also lengthens and becomes more tortuous.
• After the obstruction has been relieved, the chronically obstructed ureter becomes less dilated but never returns to normal. Similarly, because the atrophic renal parenchyma does not regenerate, even after relief of obstruction, the kidney becomes small. This is called postobstructive atrophy. The outline of the atrophic kidney remains smooth, and some dilatation of the collecting system is always present.
• Intravenous pyelogram shows delayed opacification of the collecting system and ureter in patients with mild to moderate hydronephrosis. As the degree of hydronephrosis increases, the excretion becomes progressively delayed until the kidney is not visualized at all.
• Noncontrast CT shows hydronephrosis as a dilated, fluid-filled collecting system in the renal sinus. The dilated ureter can be followed in the paravertebral region to the point of obstruction. Slower passage of contrast through the affected collecting system and ureter may be seen on contrast-enhanced phases and CT urography.
• Magnetic resonance (MR) imaging shows the dilated collecting system and ureter as fluid-filled structures with a characteristic shape and location. MR urography may be useful in identifying the level of obstruction.
If one kidney is obstructed, always determine the status of the other kidney.
Once obstruction has been diagnosed in any hollow viscus, always try to determine the level, cause, and completeness of the obstruction.
A 34-year-old woman with flank pain and fever.
Contrast-enhanced computed tomography (CT) images of the abdomen at the level of the kidneys obtained during the excretory phase. (A) The right kidney is enlarged and shows randomly scattered wedge-shaped areas of mildly decreased perfusion (arrowheads in A and B). These areas involve the entire thickness of the renal parenchyma from the renal sinus to the cortical surface. (B) Perinephric stranding is present (arrow). No fluid collection is seen in the renal parenchyma or perinephric space. The renal outlines are normal. There is no hydronephrosis.
• Acute pyelonephritis: The characteristic finding is unilateral or bilateral renal enlargement with areas of mildly decreased perfusion. These areas are randomly scattered and involve the parenchyma from the renal sinus to the cortical surface.
• Renal infarcts: Multiple renal infarcts also have the appearance of perfusion defects involving the entire parenchyma and may mimic acute pyelonephritis. However, the perfusion defects due to infarcts are well defined and larger, with a complete absence of perfusion. If necessary, delayed repeat scanning can be performed, which will show no contrast accumulation in the perfusion defects, whereas in acute pyelonephritis, these areas will become denser. In subacute or chronic cases, the affected kidney is smaller.
• Delayed nephrogram from ureteric obstruction: In patients with acute ureteric obstruction, the passage of contrast through the affected kidney is delayed. Therefore, while the normal, contralateral kidney may be in the nephrographic phase, the affected kidney is still in the corticomedullary phase. The unenhanced renal pyramids in the corticomedullary phase may superficially resemble the perfusion abnormality of acute pyelonephritis. However, their regular distribution around the renal sinus and their separation from the renal surface by the enhanced renal cortex allows a differentiation between the two entities.
• Acute pyelonephritis is a common condition caused by ascending urinary tract infection. It is more frequent in women. Escherichia coli is the organism most often responsible for the ascending type of infection. Less commonly, infection may spread to the kidneys through a hematogenous route. In such cases, the causative organisms are mostly Gram-positive cocci.
• Acute pyelonephritis may be bilateral or unilateral, and it may even involve a part of the kidney. In these cases, the term focal acute pyelonephritis is used.
• Clinical features of dysuria, flank pain, fever, leukocytosis, and positive urine cultures are sufficiently characteristic that the diagnosis is often made clinically. Imaging is necessary only if the clinical diagnosis is in doubt, episodes are recurrent, or there are risk factors for or a clinical suspicion of the development of complications.
• The affected kidney is enlarged, and areas of relative ischemia develop within the kidney as the result of increased intraparenchymal pressure. Perinephric edema may be present.
• If treated early in its course, acute pyelonephritis responds well to antibiotics, with the clinical features resolving within a few days. The resolution of imaging findings may lag that of the clinical features by 4 to 6 weeks. Morphologically, the kidneys return to normal without any permanent sequelae.
• In some patients, acute pyelonephritis may be complicated by the development of a renal or perinephric abscess. This is more common in patients with diabetes or immunosuppression.
• Intravenous pyelogram is normal in mild cases; in severe cases, the affected kidney may not be visualized.
• Ultrasound may be normal or may show swollen kidneys areas of increased or decreased echogenicity. The most dramatic findings are seen on power imaging, which shows absence of flow similar to contrast-enhanced CT findings.
• Noncontrast CT shows unilateral or bilateral renal enlargement with or without perinephric stranding. Findings on noncontrast CT may resemble those of ureteric stone disease. However, the involvement is more likely to be bilateral in acute pyelonephritis, and obstructive changes of the collecting system are not expected.
• Magnetic resonance findings are nonspecific in the form of enlarged kidneys and wedge-shaped areas of increased intensity on T2-weighted images.
Although the infection always involves the collecting system, imaging signs like wall thickening, debris, and peripelvic and periureteric stranding are seen much less commonly.
Acute pyelonephritis can be easily missed if the kidneys have been imaged in the corticomedullary phase.
Perinephric stranding is frequently seen in normal, symptomless older adults. Therefore, be careful in attaching significance to this if there are no other associated findings of acute pyelonephritis or obstruction.
A 58-year-old man who has diabetes presents with acute bilateral flank pain and hematuria.
Ten-minute intravenous pyelogram (IVP) image of the kidney area shows that both kidneys are normal in size, shape, position, orientation, and outline. Many of the calices show extracaliceal collections of contrast, some of which are round (arrowheads), others flame-shaped (arrows). Opacified pelves and visualized upper ureters on both sides are normal in caliber and outline without filling defects.
• Renal papillary necrosis: The characteristic features on IVP are contrast-filled cavities and fissures in the papillae. Various terms (e.g., “ball-on-T” “flame-shaped”) have been used to describe the various shapes of the extracaliceal contrast collections. In later stages, the papillae slough off. A sloughed papilla may cause a filling defect within the contrast-filled collecting system and ureter. The calices whose papillae have sloughed off have a flat or convex appearance.
• Renal tuberculosis: Multiple extracaliceal contrast collections are also found in renal tuberculosis. They are usually not limited to the renal papillae, are irregular, and may be associated with calcifications in the renal parenchyma.
• Hydronephrosis: This may resemble renal papillary necrosis because of the convex appearance of the calices. However, a hydronephrotic kidney also shows dilatation of the infundibulum and pelvis, which is not seen in renal papillary necrosis in the absence of obstruction.
• Acute papillary necrosis is characterized by destruction of the renal papillae. It is caused by an ischemic or chemical injury to the renal papillae. Infection may play a role. The papillae are particularly vulnerable to this kind of injury because of their already tenuous blood supply and high salt content.
• Conditions that predispose to acute renal papillary necrosis are analgesic nephropathy, dehydration, diabetes mellitus, urinary tract infection, and sickle cell disease.
• Clinical features include the sudden onset of flank pain, fever, and hematuria. Sloughed off papillae can cause ureteric colic. In patients with diabetes, a sudden deterioration of renal function should raise the possibility of acute papillary necrosis. Rarely, it may be an incidental finding.
• Pathologically, there is necrosis of some or all of the papillae, often bilaterally. This leads to clefts, fissures, and cavities within and around the papillae. Ultimately, the affected papillae may slough off. The imaging findings reflect the pathologic process, with excreted contrast filling the spaces created by clefts, fissures, cavities, and papillary sloughing. Papillae that remain in situ may calcify with time. Different stages may be seen in the same kidney.
• Treatment is supportive.
• Plain kidney-ureter-bladder (KUB) radiograph is typically normal. In chronic cases, calcified papillae may be seen over the renal shadows and be mistaken for stones.
• Retrograde pyelography may show ureteric obstruction by a sloughed papilla. More commonly, extracaliceal contrast is seen, as on IVP.
• Sonography is usually normal. In advanced cases, it may show cavities in the tips of the pyramids left behind by sloughed papillae. Calcifications at papillary tips may be seen in chronic cases as echogenic shadowing foci. They are impossible to differentiate from stones.
• Noncontrast computed tomography (CT) may detect obstructive changes due to a sloughed papilla in the acute stages and calcifications of the papillae in chronic stages. Contrast-enhanced CT may show ill-defined areas of ischemia in the papillary tip in early stages, even when an IVP appears normal. These may resolve completely. In florid cases, the kidneys may show an edematous appearance on CT. Findings on CT urography resemble those on IVP, with the typical changes of extracaliceal contrast in various configurations and caliceal deformity. Classic descriptive names (e.g., “claw sign,” “ring sign,” “forniceal clefts,” “flame-shaped collections of contrast,” and “ball-on-T appearance”) are used to describe the papillary changes and caliceal deformity of papillary necrosis seen on IVP as well as the excretory phase of CT-IVP.
• In early stages, while the IVP is normal, contrast-enhanced CT shows decreased perfusion of the papillae, best seen in the nephrographic phase.
Because of the subtlety of the imaging findings of renal papillary necrosis, always consider the diagnosis of renal papillary necrosis and look for characteristic signs if an IVP examination looks normal.
A 38-year-old woman who underwent contrast-enhanced computed tomography for vague abdominal pain.
(A) Contrast-enhanced computed tomography (CT) image of the abdomen at the level of the kidneys obtained during the nephrographic phase shows that the kidneys are malrotated, with the renal hila pointing forward (arrows). No abnormality of size, shape, location, outline, or parenchymal thickness is present. (B) Contrast-enhanced CT images of the abdomen at a level lower than that of Figure A shows that the lower poles of both kidneys are joined by an isthmus, which is the bar of enhancing renal tissue crossing the spine (arrow). The ureters can be identified anterior to this isthmus (arrowheads).
• Horseshoe kidney: The characteristic feature on CT is an isthmus that always connects the lower poles of both kidneys. It may vary from a thin fibrotic strand to full parenchymal thickness.
• Simple nonrotation: In one or both kidneys, the renal sinus may point anteriorly. However, there is no connecting isthmus.
• Retroperitoneal fibrosis: If the plaque in the retroperitoneum is thick, it may resemble horseshoe kidney. However, the plaque is seen to be separate from the kidneys and does not contain normal renal tissue. The ureters run behind rather than anterior to the plaque.
• Horseshoe kidney is a common congenital anomaly in which a bar of tissue, called the isthmus, connects the lower poles of the kidneys.
• It is caused by a failure of the metanephric blastema to separate into two kidneys.
• Horseshoe kidney is usually an incidental finding on imaging. Horseshoe kidney is prone to develop the same pathologic conditions that affect normally developed kidneys. Nontraumatic pathology in horseshoe kidney is not more common than in normal kidneys. However, because the kidney is abnormally placed, it is more prone to trauma.
• The isthmus of a horseshoe kidney may vary in thickness, depending on the amount of functioning renal parenchyma within it. On one extreme, it may be a fibrous band; on the other, it may have full-thickness renal parenchyma. The ureters pass anterior to the isthmus, and this relationship is characteristic. Accessory renal arteries supply the isthmus. Because of the presence of the isthmus, the kidneys cannot rotate during development, remaining in the fetal orientation with the sinuses pointing anteriorly. The isthmus also interferes with the ascent of the kidney. Therefore, a horseshoe kidney is often lower in position than normal kidneys.
• No treatment is considered necessary. The isthmus can be divided if it is interfering with drainage of the kidney.
• Plain radiographs of the abdomen may show the horseshoe-shaped outline of the kidney but are often normal.
• On intravenous pyelogram, the isthmus can be seen on the immediate postinfusion images. However, more often, the isthmus cannot be seen. Horseshoe kidney is then recognized by nonrotation and abnormality of the renal axis. Nonrotation manifests in the form of medially pointing lower pole calices, which lie medial to the ureters. The renal axes are reversed, so that the lower poles are closer to the spine than are the upper poles.
• Ultrasound shows poor definition of the lower poles of the kidneys. This should prompt an examination from the anterior aspect of the abdomen to show the isthmus running anterior to the aorta and inferior vena cava.
• On magnetic resonance imaging, the findings resemble those on CT. If renal tissue is present in the isthmus, it follows the signal characteristics of normal renal tissue. If the isthmus is composed of a fibrous band, it is hypointense on T1- and T2-weighted images.
If both kidneys are malrotated on CT, a careful search should be made for the isthmus to establish the diagnosis of horseshoe kidney.
A 31-year-old man with recurrent urinary tract infection.
(A) Precontrast axial computed tomography (CT) image at the level of the urinary bladder shows two thick-walled, fluid-filled structures lying posterior to the urinary bladder (arrows). No calcifications are seen within their lumina. No fat stranding is seen in the pelvis. (B) Postcontrast axial CT image obtained in the excretory phase at the same level as Figure A shows excreted contrast in the left fluid-filled structure (arrow), thus demonstrating communication with the urinary tract. No filling defect is seen. (C) Postcontrast axial CT image obtained in the excretory phase at a level below that of Figures A and B shows excreted contrast in the right fluid-filled structure (arrow). The lower ends of the ureters (arrowheads) are seen to be intimately related to the abnormalities close to where they insert into the urinary bladder.
• Hutch diverticula: These are congenital outpouchings arising from the urinary bladder. The existence of communication can be deduced indirectly from the presence of excreted contrast on contrast-enhanced excretory phase images. A location adjacent to the ureterovesical junction is characteristic.
• Acquired bladder diverticula: These are outpouchings of the urinary bladder mucosa, usually with an underlying cause. Their location is random and not related to the ureteric orifices. Their walls are characteristically thin.
• Pelvic fluid collections: Abscesses show thick enhancing walls and inflammatory changes. Lymphoceles are bland spherical fluid collections located in the external or internal iliac lymph node region. Seminal vesicle cysts are small and intimately related to the seminal vesicles. None of these entities fill with excreted contrast.
• Bladder diverticula are outpouchings arising from the bladder wall and communicating with the bladder cavity.
• Bladder diverticula may be congenital or acquired. Congenital diverticula are usually solitary and occur in specific locations. They may be at the apex of the bladder if a urachal remnant has remained partially patent at its origin from the bladder (urachal diverticulum). Hutch diverticulum, which may be unilateral or bilateral, is a congenital diverticulum located close to the ureterovesical junction. Acquired diverticula are caused by bladder outlet obstruction or neurogenic bladder.
• Bladder diverticula are usually an incidental finding on imaging. They may manifest as recurrent urinary tract infections due to stasis of urine. Hutch diverticulum is a cause of vesicoureteric reflux in boys and young men. This results in recurrent urinary tract infections and reflux nephropathy.
• Stones or urothelial neoplasms may develop in diverticula.
• On pathologic examination, the diverticula are of varying sizes. The neck may be small or large. The wall is made up of all three layers of the bladder in congenital diverticula and prolapsed mucosa in acquired diverticula.
• Diverticula are surgically treated if they are large, cause symptoms, or lead to complications. Otherwise, treatment is targeted at the underlying condition.
• Diverticula fill with contrast on the excretory phase of CT urography, indirectly demonstrating communication with the urinary tract. Because the communication of a diverticulum with the urinary bladder may be small, its direct demonstration on CT may be difficult. However, a review of thin sections may be helpful. Otherwise, the diagnosis is presumed because of the proximity of the diverticulum to the urinary bladder.
• On all imaging modalities, bladder diverticula appear as solitary or multiple fluid-containing structures of various sizes that connect with the urinary bladder. Depending on its size, the communication may or may not be visible. If it is not visible directly, the communication can be deduced indirectly on intravenous pyelogram (IVP) from the passage of contrast into the diverticulum. On IVP and ultrasound, enlargement of the diverticulum on postvoid images is also an indirect sign of communication with the bladder.
When bladder diverticula are seen, always look for a cause of bladder outlet obstruction and evaluate the kidneys and ureters for hydronephrosis and hydroureter, respectively.
Always examine diverticula carefully for focal wall thickening or filling defects that may suggest malignancy.
