Lower Urinary Tract Obstruction

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What is fetal lower urinary tract obstruction?

Lower urinary tract obstruction (LUTO) is a condition in which the fetal bladder outlet is blocked. This can be due to a small membrane (posterior urethral valves) blocking the tube connecting the bladder to the genitalia (urethra) or due to complete absence of the urethra (urethral atresia). As a consequence of this bladder blockage, the fetus is unable to urinate and its bladder becomes very distended. The accumulating urine causes back pressure into the kidneys and can damage the kidney tissue. Additionally, as the fetus is not urinating, there is no amniotic fluid (oligohydramnios). Amniotic fluid is very important for fetal lung development and to allow fetal movement. A fetus lacking amniotic fluid will often have underdeveloped lungs (pulmonary hypoplasia) and may develop deformities of the limbs. This combination of findings is often called the ’Potter sequence’.

LUTO occurs in 2-3 per 10,000 pregnancies. The exact reason for the disease is unknown, but in some cases, LUTO occurs in the setting of a chromosomal anomaly or genetic syndrome.

What is the outcome for a fetus with LUTO?

The outcome of a fetus with LUTO depends on the severity of the oligohydramnios, how early it develops and the severity of the kidney damage.

When the bladder outlet is not completely blocked, the amniotic fluid is only mildly decreased and kidney damage may not be very severe. The lungs will be sufficiently developed for the child to survive after birth. Close surveillance of kidney function after birth will be required yet these children can have a normal life. Kidney function may however worsen over time and the lifetime risk of end-stage kidney disease requiring dialysis or a kidney transplant is 30%. Some of these children will also have abnormal bladder function, leading to urine retention or involuntary leaking of urine (incontinence). Children with severe kidney disease may grow more slowly than expected.

When the bladder outlet is completely blocked, the oligohydramnios is often extreme, leading to severe pulmonary hypoplasia. The lungs of these babies will be too small to allow for adequate oxygen uptake at birth and thus these babies have a high risk of dying soon after birth. Kidney function is also expected to be worse in these fetuses and the risk of end-stage kidney disease, requiring dialysis or transplant, is very high.

What other tests should we consider?

Every fetus with suspected LUTO needs a detailed ultrasound in a specialized perinatal center, such as the fetal medicine unit at Mount Sinai Hospital, to determine the exact nature of the problem and to rule out anomalies of the other fetal organs. Ultrasound will also be used to take a detailed look at the fetal kidneys to rule out other kidney anomalies. Sometimes, a detailed heart ultrasound (echocardiogram) may be required. Amniocentesis will often be suggested to determine the fetal karyotype and exclude chromosomal problems. Amniocentesis may also help in determining the fetal gender. Fetal kidney function is hard to predict before birth, but in some cases a fetal urine sample or fetal blood sample  may give additional information.

Serial ultrasounds are used to monitor the amount of amniotic fluid and the appearance of the fetal bladder and kidneys.

What therapies are available?

Fetuses in whom the amniotic fluid is normal, or only mildly decreased, do not need any therapy before birth. These babies can usually be delivered in the local hospital. After birth, the infant will usually be started on antibiotics to prevent urinary tract infections. Kidney function will be assessed by the paediatrician (doctor specialized in the care of children) and a kidney ultrasound will be organized after birth. The baby may need to be referred on a non-urgent basis to a kidney specialist (nephrologist) or a kidney surgeon (urologist) at the Hospital for Sick Children for further assessment and follow-up. If posterior urethral valves are present, these may need to be treated surgically.

In fetuses with little or no amniotic fluid (anhydramnios), a prenatal intervention called ‘bladder shunt’ may be considered. This procedure consists of inserting a special catheter into the fetal bladder. This catheter connects the bladder to the amniotic cavity, bypassing the urethra and allowing the urine to drain from the bladder. Alternatively, a fetal cystoscopy can sometimes be performed. In this procedure, a small camera is inserted through the maternal abdominal wall into the uterus and the fetal bladder. If the obstruction at the level of the urethra is identified and if posterior urethral valves are present, they can sometimes be removed with laser energy.

After bladder shunting or a fetal cystoscopy, if the kidneys are not too damaged, the amount of amniotic fluid may improve, thereby helping lung growth and possibly increasing the chance of survival after birth. The kidney damage that has occurred however is irreversible, and many of these infants will be born with moderate to severe kidney dysfunction. After birth these children will also need a procedure to create a connection between the bladder and the genitalia. In the case of posterior urethral valves, a small surgery may be needed to remove the valves. If the bladder obstruction was due to urethral atresia, more complex surgeries are needed to allow for bladder drainage.

Bladder shunting is associated with an increased risk of breaking the water early and preterm birth. The average gestational age at delivery after bladder shunting is 35 weeks. Shunts can get displaced or blocked. This happens in about one in three cases and may sometimes require a repeat procedure. Survival after bladder shunting ranges between 50-90%. One in three survivors has end-stage kidney disease by the age of five years. Survivors may also have other lung and growth problems but their self-reported quality of life falls within the normal range.

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