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Dx-Direct gets to the point! Dx-Direct is a series of eleven Thieme books covering the main subspecialties in radiology. It includes all the cases you are most likely to see in your typical working day as a radiologist. For each condition or disease you will find the information you need -- with just the right level of detail. Dx-Direct gets to the point: Definitions, Epidemiology, Etiology, and Imaging Signs Typical Presentation, Treatment Options, Course and Prognosis Differential Diagnosis, Tips and Pitfalls, and Key References All combined with high-quality diagnostic images. Whether you are a resident or a trainee, preparing for board examinations or just looking for a superbly organized reference: Dx-Direct is the high-yield choice for you! The series covers the full spectrum of radiology subspecialties including: Brain, Gastrointestinal, Cardiac, Breast, Genitourinal, Spinal, Head and Neck, Musculoskeletal, Pediatric, Thoracic, Vascular

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Veröffentlichungsjahr: 2008

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Direct Diagnosis in Radiology

Urogenital Imaging

Bernd Hamm, MD

Professor and ChairmanDepartment of Radiology, Campus MitteDepartment of Radiotherapy, Campus Virchow-KlinikumCharité – Universitätsmedizin BerlinBerlin, Germany

Patrick Asbach, MD

Department of RadiologyCharité – Universitätsmedizin BerlinBerlin, Germany

Dirk Beyersdorff, MD

Associate ProfessorDepartment of RadiologyCharité – Universitatsmedizin BerlinBerlin, Germany

Patrick Hein, MD

Department of RadiologyCharité – Universitätsmedizin BerlinBerlin, Germany

Uta Lemke, MD

Department of RadiologyCharité – Universitätsmedizin BerlinBerlin, Germany

233 Illustrations

ThiemeStuttgart • New York

Library of Congress Cataloging-in-PublicationData

Urogenitales system. English.

Urogenital imaging/Bernd Hamm... [et al.];[translator, Bettina Herwig].

p.; cm. – (Direct diagnosis in radiology)

Translation of: Urogenitales system/Bernd Hamm... [etal.].2007.

Includes bibliographical references.

ISBN 978-3-13-145151-4 (alk. paper)

1. Genitourinary organs-Radiography-Handbooks, manuals, etc. I. Hamm, Bernd, Prof. Dr. II. Title. III. Series.

[DNLM: 1. Female Urogenital Diseases-radiography-Handbooks. 2. Male Urogenital Diseases-radiography-Handbooks. 3. Diagnosis, Differential-Handbooks. 4. Urography-Handbooks. WJ 39 U775 2008a]

RC874.U73513 2008

616.6'07572–dc22

2008002212

This book is an authorized and revised translation of the German edition published and copyrighted 2007 by Georg Thieme Verlag, Stuttgart, Germany. Title of the German edition: Pareto-Reihe Radiologie: Urogenitales System.

Translator: Bettina Herwig, Berlin, Germany

Illustrator: Markus Voll, Munich, Germany

© 2008 Georg Thieme Verlag KGRüdigerstrasse 14, 70469 Stuttgart, Germanyhttp://www.thieme.deThieme New York, 333 Seventh Avenue,New York, NY 10001, USAhttp://www.thieme.com

Cover design: Thieme Publishing GroupTypesetting by Ziegler + Müller,Kirchentellinsfurt, GermanyPrinted by APPL, aprinta Druck,Wemding, Germany

ISBN 978-3-13-145151-4(TPS, Rest of World)

1 2 3 4 5 6

Important note: Medicine is an ever-changing science undergoing continual development. Research and clinical experience are continually expanding our knowledge, in particular our knowledge of proper treatment and drug therapy. Insofar as this book mentions any dosage or application, readers may rest assured that the authors, editors, and publishers have made every effort to ensure that such references are in accordance with the state of knowledge at the time of production of the book.

Nevertheless, this does not involve, imply, or express any guarantee or responsibility on the part of the publishers in respect to any dosage instructions and forms of applications stated in the book. Every user is requested to examine carefully the manufacturers' leaflets accompanying each drug and to check, if necessary in consultation with a physician or specialist, whether the dosage schedules mentioned therein or the contraindications stated by the manufacturers differ from the statements made in the present book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. Every dosage schedule or every form of application used is entirely at the user's own risk and responsibility. The authors and publishers request every user to report to the publishers any discrepancies or inaccuracies noticed. If errors in this work are found after publication, errata will be posted at www.thieme.com on the product description page.

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.

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, preparation of microfilms, and electronic data processing and storage.

Contents

1 Kidneys and Adrenals

P. Hein, U. Lemke, P. Asbach

Renal Anomalies

Medullary Sponge Kidney

Accessory Renal Arteries

Renal Artery Stenosis (RAS)

Renal Infarction

Renal Vein Thrombosis

Renal Trauma/Injuries

Acute Pyelonephritis

Chronic Pyelonephritis

Xanthogranulomatous Pyelonephritis

Pyonephrosis

Renal Abscess

Renal Tuberculosis

Renal Cysts I (Simple, Parapelvic, Cortical)

Renal Cysts II (Complicated, Atypical)

Polycystic Kidney Disease

Angiomyolipoma

Hypovascular Renal Cell Carcinoma

Oncocytoma

Renal Cell Carcinoma

Cystadenoma and Cystic Renal Cell Carcinoma

Renal Lymphoma

Renal Involvement in Phakomatoses

Kidney Transplantation I

Kidney Transplantation II

Adrenocortical Hyperplasia

Adrenal Adenoma

Adrenocortical Carcinoma

Pheochromocytoma

Adrenal Metastasis

Adrenal Calcification

Adrenal Cysts

2 The Urinary Tract

P. Asbach, D. Beyersdorff

Ureteral Duplication Anomalies

Megaureter

Ureterocele

Anomalies of the Ureteropelvic Junction

Vesicoureteral Reflux (VUR)

Acute Urinary Obstruction

Chronic Urinary Obstruction

Retroperitoneal Fibrosis

Urolithiasis

Ureteral Injuries

Urothelial Carcinoma of the Renal Pelvis and Ureter

Bladder Diverticula

Urothelial Carcinoma of the Bladder

Male Urethral Strictures

Female Urethral Pathology

Vesicovaginal and Vesicorectal Fistulas

The Postoperative Lower Urinary Tract

Bladder Rupture

Urethral and Penile Trauma

3 The Male Genitals

U. Lemke, D. Beyersdorff, P. Asbach

Scrotal Anatomy

Hydrocele

Testicular and Epididymal Cysts

Testicular Microlithiasis

Epididymoorchitis

Testicular Tumors

Testicular Torsion

Testicular Trauma

Varicocele

Benign Prostatic Hyperplasia (BPH)

Prostatitis

Prostate Cancer

Penile Cavernosal Fibrosis

Peyronie Disease

Penile Malignancies

4 The Female Genitals

U. Lemke, D. Beyersdorff, P. Asbach

Anatomy of the Uterus and Vagina

Congenital Uterovaginal Anomalies

Cysts of the Cervix, Vagina, and Vulva

Leiomyomas

Adenomyosis

Endometrial Polyps

Endometriosis

Endometrial Carcinoma

Cervical Cancer

Vaginal Carcinoma

Vulvar Carcinoma

Pelvic Organ Prolapse

Ovarian Cysts

Polycystic Ovaries

Ovarian Teratoma

Ovarian Cystadenomas

Ovarian Cancer

Ovarian Fibromas

Index

Abbreviations

3D

Three-dimensional

ACKD

Acquired cystic kidney disease

ACTH

Adrenocorticotropic hormone

ADPKD

Autosomal dominant polycystic kidney disease

ARPKD

Autosomal recessive polycystic kidney disease

BPH

Benign prostatic hyperplasia

bSSFP

Balanced steady-state free precession

CIN

Cervical intraepithelial neoplasia

CMV

Cytomegalovirus

CNS

Central nervous system

CT

Computed tomography

CTA

CT angiography

CTU

CT urography

DTPA

Diethylene triamine pentaacetic acid

EPO

Erythropoietin

ESWL

Extracorporeal shock wave lithotripsy

FDG

Fluoro-18-deoxyglucose

FIGO

Fédération Internationale de Gynécologie et d'Obstetrique

FSH

Follicle-stimulating hormone

GnRH

Gonadotropin-releasing hormone

GRE

Gradient echo

HIV

Human immuno-deficiency virus

HLA

Human leukocyte antigen

HNPCC

Hereditary nonpolyposis colorectal cancer

HPV

Human papilloma virus

HU

Hounsfield unit

IR

Inversion recovery

IVP

Intravenous pyelogram

KUB

Kidneys, ureters, and bladder

LH

Luteinizing hormone

MEN

Multiple endocrine neoplasia

MHC

Major histocompatibility complex

MIP

Maximum intensity projection

MPR

Multiplanar reconstruction

MRA

Magnetic resonance angiography

MRI

Magnetic resonance imaging/image

NHL

Non-Hodgkin lymphoma

PCR

Polymerase chain reaction

PD

Proton density

PET

Positron emission tomography

PI

Pulsatility index

PSA

Prostate-specific antigen

PTA

Percutaneous transluminal angioplasty

PTH

Parathormone

RAS

Renal artery stenosis

RCC

Renal cell carcinoma

RI

Resistance index

SE

Spin echo

SIL

Squamous intraepithelial lesion

TIRM

Turbo inversion recovery magnitude

TRAS

Transplant renal artery stenosis

TSE

Turbo spin echo

TURB/TURBT

Transurethral resection of bladder tumor

TURP

Transurethral resection of the prostate

UAE

Uterine artery embolization

UPJ

Ureteropelvic junction

UTI

Urinary tract infection

UVJ

Ureterovesical junction

VCUG

Voiding cystourethrogram

VIN

Vulvar intraepithelial neoplasia

VUR

Vesicoureteral reflux

1 Kidneys and Adrenals

Renal Anomalies

Definition

Etiology

Renal ectopia: During embryogenesis the developing kidneys ascend from the true pelvis into the lumbar region Failure to ascend results in renal ectopia, pelvic kidney being the most common form Less common are lumbosacral or thoracic kidneys and crossed renal ectopia with asymmetric fusion of the two kidneys on the same side of the body.

Malrotation: Common Anteriorly, laterally, or posteriorly directed renal pelvis.

Duplex kidney: Kidney with two separate pelvicaliceal systems connected by a column of renal parenchyma.

Horseshoe kidney: Kidneys fused at lower pole Ascent arrested by inferior mesenteric artery Kidneys connected by a parenchymal or fibrous isthmus Typically associated with ureteropelvic junction obstruction, ureteral duplication, and genital tract anomalies.

Imaging Signs

Modality of choice

IVP Ultrasound CT MRI.

Intravenous pyelogram findings

– Ectopic/horseshoe kidney: Location, shape.

– Duplex kidney: Two renal pelves that drain separately.

Ultrasound, CT, and MRI findings

– Pelvic kidney: Renal artery supplying the kidney arises from the aorta at a lower level or from the ipsilateral iliac artery.

– Horseshoe kidney: Mediolaterally directed parenchyma Medial position of lower calices Renal pelves face anteriorly Isthmus located anterior to the abdominal aorta and inferior vena cava and posterior to the inferior mesenteric artery Evaluation of vascular anatomy by CT after intravenous contrast administration.

– Duplex kidney: Parenchymal isthmus between separate collecting systems.

– Malrotation: Usually detected incidentally.

Clinical Aspects

Typical presentation

– Usually an incidental finding.

– Horseshoe/pelvic kidney: May be complicated by obstruction, infection, or calculus formation.

– Increased risk of injury in trauma.

– Some patients may present with secondary hypertension due to stenosis of an accessory renal artery/polar artery.

Treatment options

Symptomatic treatment.

Fig. 1.1 a–c Diagrammatic representation of major renal anomalies.

Fig. 1.2 Horseshoe kidney. Axial MPR from contrast-enhanced multislice CT. Preaortic parenchymal isthmus of the horseshoe kidney. The fused kidney is just below the inferior mesenteric artery.

Fig. 1.3 Horseshoe kidney. Coronal MIP reconstruction.

Course and prognosis

Good prognosis if there are no complications.

What does the clinician want to know?

Diagnosis Exact location Presence of complications.

Differential Diagnosis

Nephroptosis (floating/wandering kidney)

– Downward displacement of the kidney; acquired condition characterized by excessive descent of the kidney when the body is erect

– Differs from pelvic kidney in that the paired renal arteries are found in their typical locations

– If additional rotation occurs, there is the risk of vascular compression/torsion or ureteral compression with intermittent hydronephrosis

Duplicated renal pelvis

– Usually one renal pelvis drains the upper group of calices and a second drains the middle and lower groups

– The two renal pelves unite proximally

Tips and Pitfalls

Parenchymal isthmus of a horseshoe kidney can be misdiagnosed as a preaortic lymphoma on ultrasound.

Selected References

Cocheteux B et al. Rare variations in renal anatomy and blood supply: CT appearances and embryological background. A pictorial essay. Eur Radiol 2001; 11: 779–786

Medullary Sponge Kidney

Definition

A developmental abnormality characterized by cystic dilatation of the collecting tubules in the medullary pyramids. Synonyms: Renal tubular ectasia and Cacchi-Ricci disease.

Epidemiology, etiology

Prevalence: 5:10 000 to 5:100 000 More commonly affects both kidneys Rarely familial Associated with Beckwith-Wiedemann syndrome, Ehlers-Danlos syndrome, hyperparathyroidism, and congenital pyloric stenosis Etiology unknown.

Imaging Signs

Modality of choice

IVP, contrast-enhanced CT (CTIVP).

Radiographic findings (abdominal plain film—KUB)

Plain radiograph may be normal or show nephrocalcinosis/nephrolithiasis.

Intravenous pyelogram findings

– Linear densities in the renal pyramids due to ectatic tubules/cystic cavities Restricted to the papillary portion of the pyramids.

– “Paintbrush” appearance due to the presence of contrast within dilated collecting ducts (Bellini ducts) in the medullary pyramids.

– Mild ductal ectasia: Linear striations.

– Moderate ductal ectasia: Grapelike clusters of rounded cystic opacities in the papillae, enlarged papillae, splaying of the caliceal cups.

– Severe disease: Gross cystic changes with marked distortion of the calices.

– Hydronephrosis in the presence of obstruction.

CT findings

– Unenhanced CT: Normal-sized, large, or small kidney Cortical depressions in the presence of scars Multiple calcifications visible with complications such as nephrocalcinosis or nephrolithiasis Hydronephrosis in patients with obstruction.

– CT after intravenous contrast administration, CT IVP: “Paintbrush” appearance and same degrees of severity as with IVP (see “Intravenous pyelogram findings” above) Nephrocalcinosis/nephrolithiasis Determination of the site of obstruction in patients with obstructive complications.

Ultrasound findings

Pyramidal calcifications identified as hyperechoic foci with acoustic shadowing Cystic lesions.

Fig. 1.4 Medullary sponge kidney. IVP 20 minutes after contrast infusion. Marked tubular ectasia.

Clinical Aspects

Typical presentation

– Asymptomatic in the absence of complications.

– Complications: Hypercalciuria Nephrolithiasis Nephrocalcinosis.

– Clinical presentations associated with complications: Urolithiasis Recurrent hematuria Urinary tract infections Reduced maximal urinary concentrating ability Incomplete distal tubular acidosis.

Treatment options

Symptomatic treatment: Thiazides, antibiotics, ESWL.

Course and prognosis

Depend on complications.

What does the clinician want to know?

Diagnosis Detection of nephrocalcinosis/nephrolithiasis Detection and location of calculi Presence of obstruction.

Differential Diagnosis

Renal papillary necrosis

– Clinical presentation

Renal tuberculosis

– Clinical presentation, pathogen detection

Papillary blush

– Normal finding on IVP associated with contrast dose

Distal renal tubular acidosis

– In the presence of nephrocalcinosis

Primary hyperparathyroidism

– In the presence of nephrocalcinosis

Fig. 1.5 a–c Medullary sponge kidney. Multiple, partially striated, calcifications. No obstruction.

a Postcontrast axial multislice CT in the cortical phase.

b Coronal MPR from the cortical phase.

c Coronal MPR from the corticomedullary phase.

Selected References

Patriquin HB, O'Regan S. Medullary sponge kidney in childhood. AJR 1985; 145: 315–319

Thomsen HS et al. Renal cystic disease. Eur Radiol 1997; 7: 1267–1275

Accessory Renal Arteries

Definition

Epidemiology

Common anatomic variant.

Etiology

Accessory renal arteries may occur as polar arteries or as arteries entering the renal hilum.

Imaging Signs

Modality of choice

CTA MRA.

CT and MRI technique

Contrast bolus timing by means of bolus tracking or test bolus injection for optimal arterial phase imaging Acquisition of a 3D data set.

Clinical Aspects

Typical presentation

Usually asymptomatic Some patients may present with renovascular hypertension due to accessory renal artery stenosis.

Treatment options

Treatment only in symptomatic patients.

What does the clinician want to know?

Diagnosis Preoperative assessment of vascular anatomy in living kidney donors.

Tips and Pitfalls

Thin-slice data set acquired by multislice spiral CT or MRA is necessary to identify tiny accessory renal arteries.

Fig. 1.6 Multiple arteries supplying the right kidney. MIP reconstruction from contrast-enhanced multislice CT data. The individual renal arteries are indicated by arrows.

Renal Artery Stenosis (RAS)

Definition

Luminal narrowing of the renal artery.

Epidemiology, etiology

Atherosclerosis: Most common cause of RAS Luminal narrowing due to athero-sclerotic plaque with/without calcification. Plaque may have fibrotic/soft components More common in men Bilateral RAS in 30–40% of cases Athero-sclerotic RAS typically at the origin of the renal artery from the abdominal aorta.

Fibromuscular dysplasia: Second most common cause Noninflammatory fibrotic thickening of the vessel wall Typically caused by medial fibroplasia, less frequently by intimal or periarterial fibroplasia Bilateral in two thirds of cases More common in women Lesions usually affect the middle or distal segment of the renal artery No calcinosis of the vessel wall.

Rare causes: Aortic dissection/aneurysm Takayasu arteritis Polyarteritis nodosa Neurofibromatosis Retroperitoneal fibrosis Irradiation Thromboembolism Tumor compression.

Imaging Signs

Modality of choice

Color Doppler ultrasound CTA MRA.

Ultrasound findings

Peak systolic velocity ≥ 190 cm/s and RI < 0.55 indicate hemodynamically significant RAS Turbulent flow in the poststenotic segment Tardus/parvus wave-form with delayed acceleration and rounded systolic peak distal to the stenosis.

CT findings

Unenhanced CT to detect calcified plaques in the renal artery High spatial resolution and optimal bolus timing/opacification are important for CTA CT tends to overestimate stenosis.

Atherosclerosis: Concentric/eccentric stenosis Focal or segmental ostial stenosis Poststenotic dilatation may be present Identification of plaque Use of an automated vessel analysis tool can be helpful.

Fibromuscular dysplasia: Characteristic string-of-beads appearance of the artery with segmental stenoses Circumscribed dilatations/aneurysms Cortical/corticomedullary phase images will show delayed parenchymal enhancement, delayed excretion, and infarction.

MRI findings

T1-weighted 3D GRE sequence after intravenous contrast administration for MPR or MIP reconstruction Findings as on CTA.

Fig. 1.7 Renal artery stenosis. Coronal MIP from MRA data. Atherosclerotic RAS near the origin of the left renal artery.

Fig. 1.8 Angiogram. Atherosclerotic stenosis of the right renal artery.

Clinical Aspects

Typical presentation

Secondary arterial hypertension with very high blood pressure Renovascular hypertension in children or young adults suggests fibromuscular dysplasia Renovascular hypertension in adults suggests atherosclerosis Partial or complete loss of renal function Systolic/diastolic bruit over the flank.

Complications: thrombosis, dissection with renal artery occlusion and renal infarction, pulmonary edema and left ventricular decompensation in case of severe hypertension.

Treatment options

Angioplasty Vascular surgery Antihypertensive therapy.

Follow-up after treatment

CTA for follow-up after stenting (stent produces signal void on MRA).

What does the clinician want to know?

Hemodynamic relevance Parenchymal damage Interventional therapy possible?

Tips and Pitfalls

Renal artery stenosis may be overlooked if the CT/MRI slices are too thick Proper timing is important for CTA/MRA.

Selected References

Herborn CU et al. Renal arteries: comparison of steady-state free precession MR angiography and contrast-enhanced MR angiography. Radiology 2006; 239: 263–268

Leiner T et al. Contemporary imaging techniques for the diagnosis of renal artery stenosis. Eur Radiol 2005; 15: 2219–2229

Renal Infarction

Definition

Ischemic necrosis of renal parenchyma Focal or global Acute, subacute or chronic.

Etiology, pathophysiology

Causes:

Mainly caused by acute occlusion of an artery supplying the kidney due to:

– Thrombosis: Atherosclerosis Polyarteritis nodosa Conditions predisposing to thrombosis.

– Embolism: Atrial fibrillation Endocarditis Myocardial infarction Catheter angiography.

– Trauma: Blunt abdominal trauma.

Anatomic extent:

– Subsegmental or segmental infarct (occlusion of a subsegmental/segmental artery) One or more infarcted areas.

– Global infarct (occlusion of the main renal artery).

– Unilateral global infarct: Suggests thrombosis/trauma.

– Bilateral multiple (sub-) segmental infarcts: suggest embolism.

Imaging Signs

Modality of choice

Ultrasound CT MRI.

General

Extent of renal infarction can be assessed by contrast-enhanced CT/MRI or color Doppler ultrasound.

Ultrasound findings

Color Doppler ultrasound demonstrates focal or complete absence of blood flow in the renal parenchyma Can also be demonstrated by contrast-enhanced ultrasound.

CT findings

Extent of infarcted area:

– Subsegmental: Sharply demarcated, wedge-shaped area of decreased enhancement Wedge base at the renal capsule.

– Segmental: Sharply delineated Due to occlusion of a segmental artery.

– Global: Complete absence of renal enhancement No contrast excretion “Spoke wheel” enhancement pattern is occasionally seen if there is collateral supply Cortical rim sign indicates (sub-)capsular blood flow.

Acute versus chronic infarction:

– Acute: Normal-sized kidney with smooth contour Reduced enhancement confined to a sharply demarcated area or throughout the kidney No or reduced contrast excretion Cortical rim sign.

– Chronic: Irregular renal contour Small kidney due to parenchymal thinning No cortical rim sign.

Fig. 1.9 Renal infarction. Color Doppler ultrasound showing perfusion defect in the middle third of the kidney.

Fig. 1.10 Contrast-enhanced ultrasound. No uptake of contrast in the infarcted area.

Angiographic findings

Selective renal angiography Identification of the site of vascular occlusion.

MRI findings

Older infarction isointense on T1-weighted images and hypointense on T2-weighted images Parenchymal thinning Findings on contrast-enhanced T1-weighted images similar to contrast-enhanced CT.

Clinical Aspects

Typical presentation

Flank pain Hematuria Hypertension Chronic renal failure in some patients.

Treatment options

Anticoagulant therapy Angioplasty with thrombolytic therapy in patients with fresh or incomplete arterial occlusion.

Course and prognosis

Depend on the extent of infarction, underlying cause, and presence of (late) complications.

What does the clinician want to know?

Confirmation of the diagnosis Extent of infarction Bilateral infarction?

Differential Diagnosis

Pyelonephritis

– Typically less sharply demarcated hypodensities/hypointensities

– No cortical rim sign

– Clinical signs and symptoms

Lymphoma

– Lesion not wedge shaped

Selected References

Garovic VD, Textor SC. Renovascular hypertension and ischemic nephropathy. Circulation 2005; 112: 1362–1374

Suzer O et al. CT features of renal infarction. Eur J Radiol 2002; 44: 59–64

Renal Vein Thrombosis

Definition

Thrombotic occlusion of one or both main renal veins.

Etiology

– Causes in adults: Tumor Infection Nephrotic syndrome Post partum Hypercoagulable state.

– Causes in children: Shock Trauma Sepsis Conditions predisposing to thrombosis such as sickle cell anemia.

Imaging Signs

Modality of choice

Ultrasound CT MRI.

Ultrasound findings

– Acute: Kidney enlarged Color Doppler ultrasound depicts no flow in the renal vein Vascular dilatation Hypoechoic cortex due to acute edema with preserved corticomedullary differentiation.

– Chronic: Small kidney with loss of corticomedullary differentiation Hyperechoic parenchyma due to chronic degeneration (e.g., fibrosis).

CT findings

Hypodense thrombus (filling defect) in the renal vein, best appreciated in the corticomedullary phase (venous phase) after contrast administration Vascular dilatation Venous collaterals in chronic thrombosis Renal pelvis may be compressed.

MRI findings

T1-weighted sequence after intravenous contrast administration Thrombus seen as filling defect Vascular dilatation.

Clinical Aspects

Typical presentation

Acute onset Flank pain Gross hematuria.

Treatment options

Heparin therapy Anticoagulation therapy Treatment of nephrotic syndrome.

What does the clinician want to know?

Extent Parenchymal damage Identification of underlying cause if present (e.g., tumor).

Differential Diagnosis

Tumor thrombus in RCC

– Contains enhancing tumor vessels

Fig. 1.11 a, b Post-partum bilateral renal vein thrombosis.

a Axial multislice CT scan after contrast administration. Dilated left renal vein with intraluminal filling defect.

b Coronal reconstruction showing the thrombus protruding from the right renal vein into the inferior vena cava.

Fig. 1.12a, b Thrombosis of the left renal vein. The thrombus dilates the left renal vein, which crosses in front of the aorta (arrow in a).

a Unenhanced coronal T2-weighted MR image.

b Fat-suppressed T1-weighted MR venography obtained in a comparable plane after intravenous administration of a nonspecific, gadolinium-based contrast medium.

Tips and Pitfalls

Do not acquire contrast-enhanced images before proper opacification of the veins has occurred.

Selected References

Kawashima A et al. CT evaluation of renovascular disease. Radiographics. 2000; 20: 1321–1340

Renal Trauma/Injuries

Definition

Etiology

Predominant causes: blunt abdominal trauma, penetrating injuries, and iatrogenic trauma (interventional procedures, surgery).

Classification according to severity and clinical symptoms:

– Minor lesions (>80% of cases): Intrarenal hematoma Contusion Small subcapsular laceration Subcapsular hematoma Small perinephric hematoma Subsegmental infarction.

– Major lesions (10%): Large cortical laceration Large perinephric hematoma Segmental infarction Involvement of the renal sinus with extravasation of urine.

– Catastrophic injuries: Multiple parenchymal lacerations Vascular injury Involvement of the renal pedicle.

– Injury to the ureteropelvic junction (rare).

Imaging Signs

Modality of choice

CT to demonstrate hematoma, infarction, and injury to the collecting system.

Pathognomonic findings

Striated or wedge-shaped areas of reduced enhancement in the renal parenchyma Swollen kidney.

CT findings

Unenhanced CT: Hyperdense or isodense hematoma Rounded and irregular lesion indicates intrarenal contusion Crescent-shaped lesion indicates subcapsular hematoma with intact capsule Size of perirenal hematoma correlates with the extent of injury; its location corresponds to the site of parenchymal laceration.

CT after intravenous contrast administration:

– Contusion: Corticomedullary phase—rounded hypodensity in parenchyma Urographic phase—hyperdense lesion due to contrast retention in parenchyma.

– Subcapsular or perinephric hematoma: Corticomedullary phase—crescent or linear Attenuation of 40–80 HU.

– Small laceration: Corticomedullary phase—linear hypodensity Located peripherally.

– Large laceration: Corticomedullary phase—sharply demarcated, wedge-shaped hypodensity Large perirenal hematoma.

– Concomitant rupture of the collecting system: Corticomedullary phase—hypodense lesion extending into the renal sinus Urographic phase—perirenal extravasation of contrast medium Contrast excretion into the ureter may be absent.

– Multiple lacerations and vascular injuries: Cortical and corticomedullary phases—several hypodense areas Heterogeneous appearance of hematoma Escape of contrast medium indicates active arterial bleeding.

Fig. 1.13 Small focal contusion with minor capsular tear. Sagittal MPR from multislice CT after contrast administration in the cortical phase.

Fig. 1.14 Laceration with subcapsular hematoma. Axial image after contrast administration in the corticomedullary phase.

Fig. 1.15 Cortical laceration with perinephric hematoma. Axial contrast-enhanced CT scan in the urographic phase showing involvement of the renal pelvis.

– Rupture of the ureteropelvic junction: Cortical/corticomedullary phase—normal enhancement of renal parenchyma and normal contrast excretion Urographic phase—perirenal urine leakage and opacified urinoma.

– Subsegmental renal infarction: Wedge shaped Hypodense Cortical.

– Segmental renal infarction: Reduced contrast accumulation in anterior/posterior aspect, upper/lower pole Cortical rim sign.

– Global renal infarction: Secondary to renal artery avulsion or acute renal artery stenosis Entire kidney is hypodense, indicating little or no perfusion.

Clinical Aspects

Typical presentation

Hematuria Flank pain Tenderness Anemia Shock Involvement of other organs Bone trauma.

Complications: Uremia Infection with abscess or sepsis intramural arteriovenous fistula Possible formation of hypertension, chronic Late sequelae include infection, and hydronephrosis.

Treatment options

– Minor injury: Conservative.

– Major injury: Usually treated conservatively but occasionally requires surgery.

– Catastrophic injury: Surgery.

– Active bleeding: Interventional embolization.

– Renal artery thrombosis: Anticoagulant treatment.

– Extravasation of urine: Drainage, ureteral stent.

Course and prognosis

Depend on severity of injury and complications.

What does the clinician want to know?

Severity of renal injury Involvement of the collecting system.

Tips and Pitfalls

Urinoma or rupture of the collecting system may be overlooked unless urographic phase images are obtained.

Selected References

Harris AC et al. CT findings in blunt renal trauma. Radiographics 2001; 21: 201–214

Kawashima A et al. Imaging of renal trauma: a comprehensive review. Radiographics 2001;21:557–574

Acute Pyelonephritis

Definition

An acute bacterial infection of the renal collecting system and parenchyma.

Epidemiology

Three times more common in women than men Peak incidence during the first 3 years of life.

Etiology

Ascending UTI Hematogenous spread (rare, occasionally in patients with sepsis) Focal or diffuse Predisposing factors: VUR, diabetes, pregnancy, immunocompromised status, urolithiasis Most common pathogen: Escherichia coli.

Imaging Signs

Modality of choice

CT MRI Ultrasound (mainly for follow-up).

CT and MRI findings

Swollen and edematous kidney Corticomedullary differentiation reduced or segmentally lost Striated, segmental or wedge-shaped, areas of diminished enhancement on postcontrast CT or MRI Increased contrast accumulation in the wall of the renal pelvis and ureter with induration of surrounding tissue Perirenal fluid.

Ultrasound findings

Enlarged kidney Inhomogeneous echotexture of renal parenchyma.

Intravenous pyelogram findings

Delayed and reduced opacification of the kidney Caliceal effacement caused by swelling of adjacent parenchyma Papillary necrosis in advanced disease.

Clinical Aspects

Typical presentation

Fever Flank pain Pyuria Hematuria Infants and children often present with nonspecific symptoms such as lethargy or poor general condition.

Treatment options

Antibiotic therapy Adequate fluid intake Abscess drainage Causal therapy of predisposing conditions where possible.

Course and prognosis

Good prognosis in most patients Poor prognosis in those rare cases where recurrent episodes lead to chronic pyelonephritis.

What does the clinician want to know?

Acute intervention (e.g., obstruction, abscess) necessary? Predisposing conditions.

Fig. 1.16 Acute focal pyelonephritis of the right kidney. Coronal reconstruction from cortical phase CT data. Segmental area of reduced enhancement in the upper pole. Mild swelling of the upper third of the kidney.

Fig. 1.17a, b Acute diffuse pyelonephritis of both kidneys. Axial (a) and coronal (b) cortical phase CT scans. Multiple segmental areas of reduced perfusion in the renal cortex (striation).

Differential Diagnosis

Renal infarction

– Kidney not enlarged

– Possible infarction of other organs (e.g., spleen)

Renal lymphoma

– Rounded lesions with reduced contrast enhancement

– May be difficult to differentiate from focal acute pyelonephritis

Renal trauma

– History

– Hematoma

– Parenchymal laceration

Xanthogranulomatous pyelonephritis

– Parenchyma replaced by fibrotic scar tissue with fatty components (CT!)

Tips and Pitfalls

Do not misdiagnose pyelonephritis as a renal tumor Carefully search for a possible underlying morphologic cause (anomaly).

Selected References

Bjerklund Johansen TE. The role of imaging in urinary tract infections. World J Urol 2004; 22:392–398

Paterson A. Urinary tract infection: an update on imaging strategies. Eur Radiol 2004; 14: L89-L100

Ramakrishnan K, Scheid DC. Diagnosis and management of acute pyelonephritis in adults. Am Fam Physician 2005; 71: 933–942

Chronic Pyelonephritis

Definition

Chronic interstitial renal infection with scar formation Involves the collecting system and renal parenchyma