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1192
P60
Ultrasound in Medicine and Biology
focalized or globalized. In acute inflammatory processes, the tendon is edematous, its echogenicity diminished and its contours are badly defined. In chronic inflammatory processes, the difference is set by calcium intratendinous deposits, which produce posterior shadowing, and important enlargement of the fiber. This guides the sonographist and s/he can recognize when the process became chronic. 1191 Sports ultrasound Peetrons P, Vanderhofstadt A, Hopitaux IRIS SUD, Belgium Ultrasound is very important in sports medicine to assess musculoskeletal lesions. The lecture will show tailored lesions for different sports such as muscle lesions for soccer, ankle sprains, wrist lesions in tennis, shoulder lesions in throwing sports, knee and thumb lesions in skiers, knee lesions in jumpers and elbow lesions in pitchers. It is very important to know the injury mechanism, very special for each sport to understand better the ultrasonic appearance of the lesions.
CONGENITAL ANOMALY 1192 Fetal hydronephrosis Filly R, University of California San Francisco, United States of America Antenatal sonography readily demonstrates both normal and abnormal fetal urinary tract anatomy. Because obstructive genitourinary lesions are common and because sonography is especially accurate for detecting fluid-filled pathologic lesions, careful evaluation of the fetal abdomen reliably detects the vast majority of fetal obstructive uropathic events. Most renal anomalies are incidental findings, however, and are not detected unless images of the kidneys and bladder are carefully obtained. The spectrum of renal pathology seen prenatally is not readily subdivided by pathophysiologic mechanisms. I prefer to think of congenital abnormalities of the fetal kidneys in two dominant categories: those abnormalities in which the fetal kidney appears “hydronephrotic” and those in which it does not. In this lecture I will concentrate on those renal abnormalities wherein the kidney appears “hydronephrotic.” Although most commonly, pathologic states that produce this appearance are obstructive uropathic events, not all such fetuses are obstructed. Conversely, many fetuses whose kidneys have been destroyed by obstructive events do not demonstrate “hydronephrosis.” Careful assessment of the sonographic features of fetal hydronephrosis usually permits localization of the level of urinary tract obstruction. This information is essential for judging prognosis and management, especially when in utero diversion of the obstruction is contemplated. The obstructive pathologies which produce a characteristic “hydronephrotic” kidney in utero are the same ones that most commonly cause this appearance in newborns: ureteropelvic junction obstruction, ureterovesical obstruction (ectopic ureterocele, UVJ stenosis and congenital megaureter) and posterior urethral valves. As well, vesicoureteral reflux can produce upper tract dilatation when of more severe grades. Among these, the pathologic event most likely to damage fetal kidneys is posterior urethral valves. The lecture will concentrate on this pathology. As the name implies, the pathologic event is obstruction of the posterior urethra by valves. Unfortunately, this relatively easily corrected obstruction can have overwhelming effects on the fetus prior to a time when surgery can be performed. Characteristically, the bladder dilates and can be massive in size. The wall becomes hypertrophied and develops trabeculation. The ureters tend to be dilated. The ureteral dilatation observed in this condition likely has several causes. Reflux is commonly demonstrated in children with posterior urethral valves.
Volume 32, Number 5S, 2006 However, as will be seen, only the mild to moderately affected fetuses survive to childhood. It is my strong belief that reflux in severe cases affecting the fetus is massive and high in pressure and likely to result in the forms of renal damage so commonly seen in fetuses with posterior urethral valvular obstruction. The kidneys commonly demonstrate hydronephrosis and the parenchyma is commonly dysplastic. Obstruction to flow of urine from the bladder results in oligohydramnios. Importantly, fetuses exposed to oligohydramnios early in pregnancy and for prolonged periods of time develop pulmonary hypoplasia that may be severe. Indeed pulmonary hypoplasia is the most common pathway to death in the neonatal period. 1193 Nonhydronephrotic fetal renal abnormalities Filly R, University of California San Francisco, United States of America Antenatal sonography readily demonstrates both normal and abnormal fetal urinary tract anatomy. Most renal anomalies are incidental findings, however, and are not detected unless images of the kidneys and bladder are carefully obtained. The spectrum of renal pathology seen prenatally is not readily subdivided by pathophysiologic mechanisms. I prefer to think of congenital abnormalities of the fetal kidneys in two dominant categories: those abnormalities in which the fetal kidney appears “hydronephrotic” and those in which it does not. In this lecture I will concentrate on those renal abnormalities wherein the kidney does not appear “hydronephrotic.” Many fetuses whose kidneys have been destroyed by obstructive events do not demonstrate “hydronephrosis.” The three principle pathologies that affect the fetal kidney wherein the term “hydronephrosis” does not come to mind are renal agenesis, multicystic dysplastic kidney and the broad category of diseases called “polycystic” disease. This lecture will concentrate on multicystic dysplasia and its discrimination from “hydronephrosis” and autosomal recessive (infantile) polycystic disease (ARPKD). Obstruction has profound effects on the fetal kidney. The earlier and more complete the obstruction, the more profound the effect. Thus, the most dramatic example is the so-called “multicystic dysplastic” kidney (MCDK) since in this condition the ureter is completely obstructed (atresia) and most commonly the renal pelvis is also atretic. This total obstruction occurs during the very formation of the kidney. In its classic form, MCDK produces a totally cystic kidney. MCDK is a nonfunctioning kidney. However, nephrons are present that produce the fluid that fills and gradually expands the cysts. But as these nephrons are destroyed or die, the fluid in the cysts gradually resorbs. In the vast majority of cases, the kidney “grows” until the nephrons die and then “shrinks” away. The natural history of MCDK not only ends with a small or absent kidney, it also “starts small.” MCDK is not recognizable until the renal cysts become macroscopically visible. Therefore, during the first and early second trimester the entity may escape detection. MCDK is associated with contralateral renal disease frequently. Although the contralateral kidney is most often normal, it may also show MCDK or be atretic: both lethal conditions. The sonographic appearance of MCDK is typical and it can be discriminated both from hydronephrosis and ARPKD (when MCDK is bilateral) in virtually all instances. As with fully developed bilateral MCDK, ARPKD also produces very large kidneys in the fetus. However, the vast majority of the renal cysts in this disease are below the limits of sonographic resolution in fetal life. Some cysts may be, and usually are, visible on the sonogram. However, the size and number of visible cysts will not account for the size of the kidney in ARPKD whereas in MCDK, the size of the kidney is always proportional to the size and number of visible cysts. This feature discriminates the two entities with a high degree of success.
Ultrasound in Medicine and Biology
focalized or globalized. In acute inflammatory processes, the tendon is edematous, its echogenicity diminished and its contours are badly defined. In chronic inflammatory processes, the difference is set by calcium intratendinous deposits, which produce posterior shadowing, and important enlargement of the fiber. This guides the sonographist and s/he can recognize when the process became chronic. 1191 Sports ultrasound Peetrons P, Vanderhofstadt A, Hopitaux IRIS SUD, Belgium Ultrasound is very important in sports medicine to assess musculoskeletal lesions. The lecture will show tailored lesions for different sports such as muscle lesions for soccer, ankle sprains, wrist lesions in tennis, shoulder lesions in throwing sports, knee and thumb lesions in skiers, knee lesions in jumpers and elbow lesions in pitchers. It is very important to know the injury mechanism, very special for each sport to understand better the ultrasonic appearance of the lesions.
CONGENITAL ANOMALY 1192 Fetal hydronephrosis Filly R, University of California San Francisco, United States of America Antenatal sonography readily demonstrates both normal and abnormal fetal urinary tract anatomy. Because obstructive genitourinary lesions are common and because sonography is especially accurate for detecting fluid-filled pathologic lesions, careful evaluation of the fetal abdomen reliably detects the vast majority of fetal obstructive uropathic events. Most renal anomalies are incidental findings, however, and are not detected unless images of the kidneys and bladder are carefully obtained. The spectrum of renal pathology seen prenatally is not readily subdivided by pathophysiologic mechanisms. I prefer to think of congenital abnormalities of the fetal kidneys in two dominant categories: those abnormalities in which the fetal kidney appears “hydronephrotic” and those in which it does not. In this lecture I will concentrate on those renal abnormalities wherein the kidney appears “hydronephrotic.” Although most commonly, pathologic states that produce this appearance are obstructive uropathic events, not all such fetuses are obstructed. Conversely, many fetuses whose kidneys have been destroyed by obstructive events do not demonstrate “hydronephrosis.” Careful assessment of the sonographic features of fetal hydronephrosis usually permits localization of the level of urinary tract obstruction. This information is essential for judging prognosis and management, especially when in utero diversion of the obstruction is contemplated. The obstructive pathologies which produce a characteristic “hydronephrotic” kidney in utero are the same ones that most commonly cause this appearance in newborns: ureteropelvic junction obstruction, ureterovesical obstruction (ectopic ureterocele, UVJ stenosis and congenital megaureter) and posterior urethral valves. As well, vesicoureteral reflux can produce upper tract dilatation when of more severe grades. Among these, the pathologic event most likely to damage fetal kidneys is posterior urethral valves. The lecture will concentrate on this pathology. As the name implies, the pathologic event is obstruction of the posterior urethra by valves. Unfortunately, this relatively easily corrected obstruction can have overwhelming effects on the fetus prior to a time when surgery can be performed. Characteristically, the bladder dilates and can be massive in size. The wall becomes hypertrophied and develops trabeculation. The ureters tend to be dilated. The ureteral dilatation observed in this condition likely has several causes. Reflux is commonly demonstrated in children with posterior urethral valves.
Volume 32, Number 5S, 2006 However, as will be seen, only the mild to moderately affected fetuses survive to childhood. It is my strong belief that reflux in severe cases affecting the fetus is massive and high in pressure and likely to result in the forms of renal damage so commonly seen in fetuses with posterior urethral valvular obstruction. The kidneys commonly demonstrate hydronephrosis and the parenchyma is commonly dysplastic. Obstruction to flow of urine from the bladder results in oligohydramnios. Importantly, fetuses exposed to oligohydramnios early in pregnancy and for prolonged periods of time develop pulmonary hypoplasia that may be severe. Indeed pulmonary hypoplasia is the most common pathway to death in the neonatal period. 1193 Nonhydronephrotic fetal renal abnormalities Filly R, University of California San Francisco, United States of America Antenatal sonography readily demonstrates both normal and abnormal fetal urinary tract anatomy. Most renal anomalies are incidental findings, however, and are not detected unless images of the kidneys and bladder are carefully obtained. The spectrum of renal pathology seen prenatally is not readily subdivided by pathophysiologic mechanisms. I prefer to think of congenital abnormalities of the fetal kidneys in two dominant categories: those abnormalities in which the fetal kidney appears “hydronephrotic” and those in which it does not. In this lecture I will concentrate on those renal abnormalities wherein the kidney does not appear “hydronephrotic.” Many fetuses whose kidneys have been destroyed by obstructive events do not demonstrate “hydronephrosis.” The three principle pathologies that affect the fetal kidney wherein the term “hydronephrosis” does not come to mind are renal agenesis, multicystic dysplastic kidney and the broad category of diseases called “polycystic” disease. This lecture will concentrate on multicystic dysplasia and its discrimination from “hydronephrosis” and autosomal recessive (infantile) polycystic disease (ARPKD). Obstruction has profound effects on the fetal kidney. The earlier and more complete the obstruction, the more profound the effect. Thus, the most dramatic example is the so-called “multicystic dysplastic” kidney (MCDK) since in this condition the ureter is completely obstructed (atresia) and most commonly the renal pelvis is also atretic. This total obstruction occurs during the very formation of the kidney. In its classic form, MCDK produces a totally cystic kidney. MCDK is a nonfunctioning kidney. However, nephrons are present that produce the fluid that fills and gradually expands the cysts. But as these nephrons are destroyed or die, the fluid in the cysts gradually resorbs. In the vast majority of cases, the kidney “grows” until the nephrons die and then “shrinks” away. The natural history of MCDK not only ends with a small or absent kidney, it also “starts small.” MCDK is not recognizable until the renal cysts become macroscopically visible. Therefore, during the first and early second trimester the entity may escape detection. MCDK is associated with contralateral renal disease frequently. Although the contralateral kidney is most often normal, it may also show MCDK or be atretic: both lethal conditions. The sonographic appearance of MCDK is typical and it can be discriminated both from hydronephrosis and ARPKD (when MCDK is bilateral) in virtually all instances. As with fully developed bilateral MCDK, ARPKD also produces very large kidneys in the fetus. However, the vast majority of the renal cysts in this disease are below the limits of sonographic resolution in fetal life. Some cysts may be, and usually are, visible on the sonogram. However, the size and number of visible cysts will not account for the size of the kidney in ARPKD whereas in MCDK, the size of the kidney is always proportional to the size and number of visible cysts. This feature discriminates the two entities with a high degree of success.