USG Evaluation of Fetal Genitourinary System

Chapter 18. USG Evaluation of Fetal Genitourinary System


3rd year resident. Jeong-Won Lee M.D.


  • Systemic approach to abnormal urinary tract


    1. Assessment of appropriateness of AFV
    2. Localization & characterization of urinary tract abnormalities
    3. Search for associated abnormalities


    • Oligohydroamnios during 2nd trimester → very poor Px. (cf. Normal AFV → good Px)
    • Polyhydramnios : mesoblastic nephroma, abnormalities of CNS, GIT.

      Cf. Polyhydramnios : in incomplete obstruction at ureteropelvic junction (d/t renal concentrating ability ↓ → UO ↑)


    • Localization & characterization of urinary tract abnormalities →
      accurate prediction of Dx & Px.


    1. Are the kidneys & bladder identified ?
    2. Is the urinary tract dilated ?
    3. Are renal cysts present or are the kidneys abnormally echogenic ?
    4. Are the GU abnormalities unilat. / bilat., and are they symmetric or asymmetric ?




    • a/w concomitant abnormalities

      ex) - Meckel-Gruber syndrome : bilateral renal cystic Dz with encephalocele.

      Jeune syndrome asphyxiating thoracic dysplasia : 25% AR recurrence risk, renal cysts in short-
      limbed dwarf with small thorax.

      VACTERL association abnormalities : Vertebral, anal, cardiac, tracheoesophageal, renal & limb)



      I. Absent visualization of kidneys



    • Absence of visualization of one or both kidney → bilat. Renal agenesis / severe hypoplasia, pelvic kidney, unilateral renal agenesis or crossed fused ectopia.



      A. Bilat. Renal agenesis or severe hypoplasia


    • 1/4000 births
    • Severe oligohydramnios, pulmonary hypoplasia, Potter faces, & contractures.
    • DDx.: bowel, adrenals (cf. Kidney → hypoechoic medullary pyramids )
    • Fetal kidney: > 10 weeks, urine production (not Major source of urine production until 14th ~ 16th week)
    • a/w ↑ numerous concomitant anomalies: CV (14%), MS (40%), CNS, GIT....



      B. Unilat. Renal agenesis



    • 4~20x than bilat.
    • Difficult Dx to confirm prenatally because adrenal or bowel in renal fossa may simulate kidney.
    • Normal AFV, fill bladder normally, good Px.
    • Contralat. Kidney : abnormally large (d/t compensatory hypertrophy)
    • a/w concomitant GU anomalies.



      C. Crossed renal ectopia, pelvic kidney, & horseshoe kidney



      1. Crossed renal ectopia


      1/7000 birth, mimic unilat. Renal agenesis on USG.

      Abnormally large & bilobed.

      Obstructive uropathy / reflux

      a/w C-V or GI abnormalities.



      2. Pelvic kidney


      1/1200 autopsy, mimic unilat. Renal agenesis

      may be identified adjacent to bladder or iliac wing

      a/w concomitant skeletal, C-V, GI, GY abnormalities.



      3. Horseshoe kidney


      1/400 persons, fusion of upper or lower poles btw 7 ~ 9 weeks.

      Frequently a/w other more serious anomalies.



      II. The urinary bladder



    • Normal fetus, bladder turnover : q 25min (7~43min throughout gestation)
    • Urine production : 20week (5cc/hr) 41 week (56cc/hr)
    • Maximal bladder volume : 20week (1cc) 41 week (36cc)
    • After 14 week, visualized in 94%.
    • Nonvisualization of bladder with normal AFV → not clinically significant & require no F/U

      Cf. In oligohydroamnios → stronger evidence for bilat. Severe renal abnormalities with ↓ urine
      production



      III. Urinary tract dilatation



    • Mainly obstruction cf. (+) obst. Uropathy in urinary tract dilatation (-)
    • Renal pelvis & kidney A-P dia.

      Assessment of degree of caliectasis → important clinical information of early & effective postnatal Mx.
    • Renal pelvic dia. < 5mm : insignificant

      5~9mm , pelvic A-P dia / kidney A-P dia < 50% → rarely to progress or to
      require postnatal Mx.

    • Renal pelvic A-P dia ≥

      10mm → abnormal < PA 24 week



      # Corteville & collegues Rx, A-P dia of renal pelvis



      1. < PA 33 week : ≥



      4mm, > PA 33 week: ≥

      7mm → F/U USG in 3~4 week



      2. If persists on prenatal exam → postnatal F/U after neonatal rehydration.



      IV. Urethral level obstruction.



    • Distal urinary tract obst. : mc from post. urethral valves.
    • Cardinal signs

      Thick-walled, dilated bladder & dilated proximal urethra

      Pelvocaliectasis, ureteroectasis, megacystis

      Oligohydramnios (if present → pul. Hypoplasia, poor Px)



      V. Ureterovesical junction obst.



      VI. Ureteropelvic junction obst.



      VII. Renal cysts.



    • Most fetuses with renal cysts



      1. MCDK (Potter type II)
      2. Obst. Uropathy resulting in renal cystic dysplasia (Potter type IV)



    • Detection of renal cysts → careful search for associated anomaly, esp in absence of features
      indicative of urinary tract obst.


    • Renal dysplasia : irreversible renal damage, functional capacity - depends on extent & severity of
      dysplasia.


    • 90% of dysplastic kidney ← result from urinary tract obst. during nephrogenesis.



      # Bernstein's classification of renal dysplasia.




      1. Multicystic dysplasia ← usually caused by ureteropelvic atresia.
      2. Focal & Segmental cystic dysplasia ← obst. Or atresia of one of ureters leading from a duplex
        kidney
      3. Cystic dysplasia a/w nonatretic urinary tract obstruction ← mc from post. urethral valves
      4. Heredofamilial cystic dysplasia.




      A. MCDK (Multicystic Dysplastic Kidney)



    • Occurs during embryogenesis ← result from atresia of ureteral bud system at level of upper 1/3 of
      ureter with concomitant atresia of renal pelvis & infundibulum


    • Some (usually very minimal) residual urine formation → but functionless


    • Renal pelvis & ureter : usually atretic & not visible


    • Typically visualizes as a paraspinous flank mass : numerous cysts of variable sizes without identifiable
      communication or anatomic arrangement


    • Change markedly in size & appearance as gestation progresses : progressive enlargement or diminution
      or may initially enlarge, then decrease later in pregnancy.


    • Bilateral MCKD: oligohydroamnios develop as early as 12weeks

      cf. Typical multicystic flank masses : visible after 16weeks.



      B. Obstructive Cystic Renal Dysplasia



    • Result from urinary tract obstruction
    • Extensive renal dysplasia : correlates with drastically reduced renal functional capacity
    • Greatly ↑ echogenecity (d/t abundant fibrous tissue)
    • DDx : MCDK → difficult


      Cystic dysplasia : Cardinal signs of urinary tract obst.

      : Recognizable parenchyma surrounds relatively small cysts

      : Bilat. (esp. distal obst) >> unilat. (ureteropelvic jx. obst)

      MCDK : Only small islands of tissue localize between predorminant cysts

      : Bilat. (20%)



      1. AR (Infantile) PCK



    • Bilat. Medullary ectasia, producing innumerable 1~ to 2~mm cysts of nonobstructive renal collecting tubules.


    • Severely affected → high mortality (d/t pulmonary hypoplasia ← oligohydroamnios)


    • Dx : as early as 16weeks, oligohydroamnios, characteristic USG finding esp. FHx(+)


    • USG : bilat. Enlarged & very echogenic kidney

      : urine within bladder (-)



      2. AD (Adult) PCK



    • As early as end of 2nd trimester
    • Kidney : normal appearance in mid 2nd trimester → become abnormal on serial exam.
    • Dx.: FHx(+), normal AFV, cystic & echogenic kidney
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