Antenatal Hydronephrosis (Urinary Tract Dilation) 

Updated: Jul 27, 2021
Author: Dennis B Liu, MD; Chief Editor: Marc Cendron, MD 


Practice Essentials

This article focuses on hydronephrosis (urinary tract dilation) that is detected by means of antenatal ultrasonography (US). This method of surveillance detects a significant fetal anomaly in 1% of pregnancies, of which 20-30% of cases are genitourinary in origin, and 50% manifest as hydronephrosis.[1, 2, 3] If not for antenatal detection by US, many of these urologic anomalies would manifest, as they did in the past, later in life as pyelonephritis, symptomatic flank or abdominal pain, renal calculi, hypertension, or even end-stage renal disease.

The degree and laterality of hydronephrosis may depend on the stage of pregnancy and the underlying etiology. US can detect the fetal bladder and kidney by 15 weeks' gestation and distinguish a central echo (renal sinus) by 18-20 weeks.[2] At 20 weeks' gestation, the fetus is larger, and an anomaly is easier to detect. Antenatal hydronephrosis has received significant attention since antenatal US became a mainstream screening tool; however, management and treatment remain controversial in terms of patient outcome.

In addition, much of the controversy stems from diagnostic dilemmas and difficulties in ascertaining which lesions are obstructive and potentially harmful to the developing fetal kidney and other organ systems affected by renal function. In general, patients with obstructive uropathy that poses a significant risk of neonatal demise due to pulmonary hypoplasia may be considered candidates for antenatal treatment.  However, antenatal management is still considered experimental.

If antenatal treatment is decided on, controversy remains regarding the efficacy of therapeutic intervention because of the limited knowledge of the underlying natural history and the difficulty of standardizing patient selection and determining appropriate outcome measures.[4] Furthermore, early diagnosis of hydronephrosis has been shown to cause significant parental anxieties during the rest of the pregnancy.[5]

With respect to terminology, the term hydronephrosis is a relatively nonspecific one and has become pejorative. Accordingly, in 2014, a multidisciplinary committee recommended use of the term urinary tract dilation instead.[6]


The ureteral bud arises from the mesonephric (wolffian) duct during the fifth week of gestation. It penetrates mesenchyme on the nephrogenic ridge, which is known as the metanephric blastema, and induces differentiation into renal parenchyma. Most nephrons are present by the middle of the second trimester, and differentiation is complete by 36 weeks' gestation.[7] The ureteral bud undergoes approximately 15 generations of division to complete the collecting system from collecting tubules proximally to the hemitrigone of the bladder distally.

Embryologically, the ureter begins development as a solid cord of tissue that lengthens and canalizes during development. Distal to the ureter, the urogenital sinus undergoes differentiation to form the bladder and urethra at 10 weeks' gestation and 12 weeks' gestation, respectively. Current technology does not allow renal imaging prior to completion of nephrogenesis.

The placenta, not the fetal kidney, functions as the fetal hemodialyzer maintaining salt and water homeostasis; however, the fetal kidney does begin producing hypotonic urine between weeks 5 and 9 of gestation and increases throughout gestation to reach rates as high as 50 mL/hr.[1]

Therefore, a deficiency at any point along the urinary tract can lead to transient or permanent partial or complete obstruction of urine flow, causing proximal dilation of the collecting system that manifests as antenatal hydronephrosis (ie, dilatation of the upper urinary tract). This obstructive process may be transient and nonpathologic and may instead be the result of normal development; however, if persistent or significant obstruction is present, nephrogenic tissue can be affected, resulting in varying degrees of cystic dysplasia, renal malformation or agenesis, and renal impairment.[8, 9]   

Most anomalies of the urinary tract discovered in the antenatal period are characterized by dilatation of the upper urinary tract. Intuitively, these lesions may be considered obstructive in nature; however, antenatal hydronephrosis can be the result of nonobstructive processes, such as vesicoureteral reflux (VUR), nonrefluxing nonobstructed megaureter, and prune belly syndrome.

Obstructive lesions, particularly bilateral lesions, are more harmful to the developing kidneys, and the urine produced is a major component of amniotic fluid necessary for normal lung development and prevention of compression deformities. Therefore, differentiation of obstructive lesions and nonobstructive lesions is extremely important in determining the eventual outcome of the fetus. However, this typically is not possible until the child is born, given that US provides little or no functional information.

Chronic partial unilateral ureteral obstruction has been experimentally demonstrated to result in significant renal maldevelopment, and early relief of the obstructive process is followed by significant hemodynamic recovery.[10, 11] Obstruction induces the renin-angiotensin-aldosterone system, causing vasoconstriction and subsequent interstitial fibrosis and ischemic atrophy, as well as induction of apoptosis in the obstructed kidney.

Josephson reported that obstruction is associated with decreased renal blood flow, glomerular filtration, and potassium excretion.[12]


Numerous pathologic entities can cause antenatal hydronephrosis (dilatation of the upper urinary tract).

Antenatal hydronephrosis without associated urinary tract anomaly is the etiology in the vast majority of infants with hydronephrosis (79-84%) and has been termed isolated antenatal hydronephrosis (IAHN). IAHN is believed to be caused by a physiologic dilatation of the developing ureter.[13]

As noted (see Pathophysiology), the ureter begins normal development as a solid cord of tissue that canalizes to allow unobstructed passage of urine. Metanephric urine production begins at approximately 8 weeks' gestation, potentially before completion of ureteral canalization. This results in transient obstruction with dilatation of the renal collecting system and ureter. Once canalization is complete, this obstruction is relieved, and dilatation may resolve.

The goal of evaluation is to differentiate benign physiologic dilatation from pathologies (eg, significant obstructive disease) that, if left untreated, would lead to renal deterioration or VUR.


United States statistics

Hydronephrosis (dilatation of the upper urinary tract) is the most common pathologic finding in the urinary tract on antenatal screening by US, accounting for 50% of all abnormal findings. The incidence varies among series because of criteria for dilatation and timing of US; however, the incidence of a significant uropathy in association with hydronephrosis is 0.2%.[14]

International statistics

International studies have supported a similar incidence, with an incidence of 0.25% in Sweden and 0.92% in Great Britain.

Age-, sex-, and race-related demographics

Studies have uniformly shown that timing of hydronephrosis is important. Early onset of hydronephrosis in fetal development is directly related to prognosis. The incidence of antenatal hydronephrosis related to sex has not been reported. No known studies report the incidence of antenatal hydronephrosis related to race.


Most neonates with antenatal hydronephrosis (dilatation of the upper urinary tract) have an excellent prognosis. In many cases, the condition resolves spontaneously, though sometimes it may signal significant urinary tract pathology.[15]

Determination of mortality is difficult with antenatal hydronephrosis because of the significant incidence of stillbirths, terminated pregnancies, and missed diagnoses, all of which lead to underestimation of the true mortality. However, most research suggests that morbidity and mortality are directly related to the underlying etiology of hydronephrosis and the effect that the lesion has on the laterality, degree, and timing of hydronephrosis and resultant oligohydramnios.

Knowledge of the natural history of each disease entity that manifests as antenatal hydronephrosis provides a better understanding and estimation of morbidity and mortality than general surveys; however, a few statements can be made.

Obstructive lesions and lesions that affect both kidneys are uniformly more threatening than nonobstructive and unilateral lesions. The survival rate with unilateral renal obstruction approaches 100%, with only 15-25% of patients requiring surgery at 4 years' follow-up.[16, 17]

In the presence of a bilateral obstructive process, oligohydramnios is the best predictor of an adverse outcome.[18, 19]  Fetal urine is a significant component of the amniotic fluid volume, and maintenance of adequate volumes is essential for normal lung development. If oligohydramnios is present, pulmonary hypoplasia and compression deformities of the skeletal system can result and significantly influence quality of life and survival (Potter syndrome).

The timing of oligohydramnios has a substantial effect on outcome. The earlier a lesion develops, the more likely it is to affect the fetal kidney, lungs, and overall outcome. In a series of 113 cases detected in the third trimester, mortality was 13%.[20]  Detection in the second trimester was almost uniformly fatal, with an 83-100% mortality.[21]  The most vulnerable period for pulmonary development is the second trimester; late-onset oligohydramnios exerts no adverse pulmonary effects.[22, 23]  In general, the major determinant of survival is pulmonary development.

Patient Education

Many fetuses have an excellent prognosis, and this should be communicated to the parents. If a fetus has findings on US that are suggestive of an adverse outcome, it is important to discuss the implications and provide the parents with information regarding further evaluation and management of their pregnancy.




The finding of antenatal hydronephrosis (dilatation of the upper urinary tract) should prompt a series of inquires regarding onset, fetal sex, oligohydramnios, laterality, severity of hydronephrosis, bladder cycling, other anomalies, prior pregnancy complications, and family history of urologic disease.

Ultrasonography (US) can provide important information, such as sex of the fetus, unilateral or bilateral disease, renal anterior-posterior (AP) pelvic diameter, bladder distention, bladder sagittal length, volume of amniotic fluid, and associated pathologic conditions. For example, Reuss et al found that 16 of 31 fetuses (55%) with bilateral hydronephrosis and oligohydramnios had an associated structural or chromosomal abnormality.[24]

Other aspects of the history that can be helpful in identifying the cause of hydronephrosis include family and maternal history.


Fetuses at highest risk for neonatal demise or pulmonary complications are those with bilateral hydronephrosis, a distended bladder, and oligohydramnios. These patients should be referred to a tertiary care center early in gestation. These neonates may require extensive cardiopulmonary support, as well as interventional support from a pediatric urologist early in the neonatal period.



Diagnostic Considerations

In addition to the conditions listed in the differential diagnosis, other problems to be considered include the following:

  • Obstructed megaureter
  • Multicystic kidney
  • Renal cystic disease
  • Megacalicosis
  • Retrocaval ureter
  • Nonrefluxing nonobstructed megaureter
  • Midureteral stricture
  • Ectopic ureter
  • Ureterocele
  • Prune belly syndrome
  • Urethral atresia
  • Anterior urethral valves
  • Cloacal abnormality
  • Hydrocolpos
  • Urachal cyst
  • Ovarian cyst
  • Bowel duplication
  • Duodenal atresia
  • Anterior meningocele
  • Pelvic tumor
  • Ureteral polyp

Differential Diagnoses



Laboratory Studies

Theoretically, a fetus with oligohydramnios and good renal function can benefit from intervention in utero. Therefore, developing methods to evaluate fetal renal function by analyzing fetal urinary components may be helpful in determining which fetuses have the most potential benefit from such intervention. With the help of ultrasonographic (US) guidance, samples of fetal urine can be obtained and analyzed. This should be performed at a specialized center that has experience in high-risk obstetrics and fetal intervention.

A retrospective review from the University of California, San Francisco, helped initiate evaluation of urine constituents as a marker of renal function into mainstream practice.[25] A healthy fetus produces hypotonic urine that becomes isotonic in the presence of progressive renal damage that impairs proximal tubular function. Elevations in urinary sodium, chloride, calcium, alpha2-microglobulin, and osmolality indicate renal injury and potentially irreversible dysplasia.[26]

Urinary calcium is currently thought to be the most sensitive predictor of renal dysplasia. These measurements are inherently difficult to evaluate because of the dynamic nature of fetal renal function; however, evaluation of multiple urinary components on serial examinations can improve diagnostic accuracy.[27]

Individual values are believed to have variable accuracy, but the combination of urinary sodium less than 100 mg/dL, osmolality less than 200 mOsm/L, and total protein less than 20 mg/dL on the third or fourth bladder tap is generally associated with normal renal function (see Table 1 below).[28] Currently, evaluation of urinary components by means of vesicocentesis is an extremely valuable tool in determining which fetuses are candidates for in-utero intervention.

Table 1. Urinary Components and Their Usefulness in Predicting Renal Dysplasia (Open Table in a new window)






Predictive Value


Predictive Value


< 100 mg/dL






< 8 mg/dL






< 200 mOsm/L






< 4 mg/dL





Total protein

< 20 mg/dL






Antenatal US is the imaging modality that originally brought the patient with antenatal hydronephrosis (dilatation of the upper urinary tract) to medical attention. This is the main diagnostic imaging method for evaluating and monitoring the fetus. Antenatal detection of fetal genitourinary abnormalities by means of US was first reported in 1970.[29]  Since then, assessment of the genitourinary system has been routine, and it should be part of every fetal US examination.

If an abnormality is found on screening or dating US, a detailed study is performed to evaluate the collecting system architecture, renal architecture and size, parenchymal echogenicity, amniotic fluid volume, and bladder fullness and function.[28]  Antenatal US is helpful in formulating a differential diagnosis of the genitourinary lesion and other coexistent fetal anomalies that can affect the treatment and clinical outcome of the fetus.

The degree of hydronephrosis is significant and can herald an obstructive process. This finding is not synonymous with the diagnosis of obstruction; however, the likelihood of having a significant urinary tract abnormality that is obstructive in nature is directly proportional to the severity of hydronephrosis.[2, 30]

Renal anterior-posterior (AP) pelvic diameter (APD) is commonly used to evaluate the significance of dilation. In one series, surgery or at least long-term monitoring for a significant urinary tract lesion was required by 94% of fetuses with a renal APD exceeding 2 cm, 50% of those with an APD of 1-1.5 cm, and only 3% of those with an APD smaller than 1 cm.[31]  In a subsequent study, a renal APD of at least 4 mm before 33 weeks' gestation and at least 7 mm after 33 weeks' gestation was considered significant.[32]  Caliectasis correlates best with the presence of a significant dilation or an obstructive process.

Grading systems in current use include the Society for Fetal Urology (SFU) system[33]  and the Urinary Tract Dilation (UTD) system.[34]  A study by Dos Santos et al found that a grading system using a combination of APD and diffuse caliectasis was able to identify children who were more likely to require surgery, particularly in the context of moderate-grade hydronephrosis.[35]  Kiener et al found that the second-trimester APD is a useful parameter for predicting the risk for postnatal surgery and recommended that the SFU grade be assessed in every antenatal US examination.[36]

The presence of a distended bladder without functional emptying is important in developing a differential diagnosis. A filled bladder should be visualized, with functional emptying observed every 30-60 minutes. A system that does not function in this manner suggests the presence of posterior urethral valves, prune belly syndrome, or the often-fatal urethral atresia.[28]  In these cases, the bladder and (sometimes) the upper urinary tract are massively dilated.

The measurement of fetal sagittal bladder length (FSBL) in combination with the presence of pelviectasis has been suggested as a tool to determine the outcome of antenatal hydronephrosis. The presence of megacystis, determined as FSBL of greater than gestational age (GA) plus 12, in association with pyelectasis, suggests the presence of posterior urethral valve or vesicoureteral reflux.[37]

Renal architecture, renal size, and renal parenchymal echogenicity are important in developing a differential and determining the potential function of the kidney. Increased echogenicity may be associated with renal dysplasia.

Caliceal anatomy revealed by US is also important to help differentiate obstructive and nonobstructive antenatal hydronephrosis. The presence of the "eggshell sign," a crescent of increased echogenicity at the caliceal-parenchymal interface, may indicate increased intrarenal pressure; thus, it is more commonly associated with obstructive processes.[38]

Differentiation between hydronephrosis and polycystic kidneys can be difficult but helpful in determining the overall survival of the fetus. Hydronephrosis tends to be an orderly process with visible connections between the dilated calices and pelvis. Polycystic kidneys do not appear as orderly, and connections between cysts are not present. Furthermore, hyperechogenicity of the renal parenchyma is more often associated with polycystic kidneys rather than hydronephrosis.

Renal size and echogenicity are also important in determining renal function. Noteworthy findings include the presence of renal cortical cysts, echogenic parenchyma, and a discernible corticomedullary junction that can herald the presence of renal dysplasia or severe and irreversible damage to the renal unit. These findings are nearly 100% specific but accurately predict dysplasia in only 60% of fetuses.[39]

Amniotic fluid volume is the single most significant determinant of fetal well-being and survival. Amniotic fluid volume is maintained by fetal urine production by 16 weeks' gestation and remains constant throughout gestation. Oligohydramnios is associated with pulmonary hypoplasia and compression deformities of the head, thorax, and extremities (Potter syndrome).

Oligohydramnios has been demonstrated to be the key factor in the development of pulmonary hypoplasia, and restoration of this fluid prevents hypoplasia. The most vulnerable period for lung development is the second trimester; late-onset oligohydramnios has little impact on overall pulmonary function.

The final consideration for the imaging team is a global assessment of the fetus. Finding abnormalities in other systems is not uncommon when a urologic abnormality is detected. One series showed that 55% of fetuses with bilateral hydronephrosis and oligohydramnios had an associated structural or chromosomal abnormality.[24]  These anomalies are commonly of cardiovascular, neurologic, and orthopedic origin, but they can be found elsewhere and should be sought during the imaging evaluation.

Magnetic Resonance Imaging

Fetal magnetic resonance imaging (MRI) is increasingly being used in the management of antenatal hydronephrosis. A study by Chalmers et al (47 patients, 88 renal units; median gestational age, 22 weeks) evaluated fetal MRI and US for this purpose in relation to various grading methods (APD, SFU, and UTD).[40]  They found that fetal MRI improved the interrater reliability of the SFU grading system and enhanced the APD intraclass correlation. MRI tended to yield a higher SFU grade than US did, but it had no significant effect on the UTD grade.

Other Tests

Chromosomal analysis can be helpful. Abnormal chromosome complement or aneuploidy is a major factor in fetal demise. Prenatal screening for aneuploidy can be accomplished by several means, including imaging techniques and maternal serum biochemistry. More invasive fetal sampling following these screening techniques is a more definitive but morbid method of confirming the diagnosis.

Normal findings on US are associated with a twofold to threefold reduction in the risk of a chromosomal abnormality as compared with the presence of minor and major abnormalities on US.[41]

Maternal serum biochemistries, such as beta human chorionic gonadotropin (β-hCG), alpha fetoprotein (AFP), and others, are used to detect aneuploidy, with a reported accuracy of approximately 65%. The best individual risk estimation is based on maternal age, US examination, and maternal biochemistry.[41]

More definitive methods of determining the presence and the exact nature of the abnormality are chorionic villus sampling and amniocentesis. The risks should be weighed against the benefits of performing the procedure.

Several studies have focused on noninvasive techniques of determining the chromosomal defect. Researchers have isolated and analyzed nucleated fetal cells from maternal blood; however, limiting factors include the relative rarity of fetal cells in maternal blood and the need to establish their fetal origin.[42] Although promising, these techniques are not yet standardized or available to the population at large.


Procedures that may be considered in the workup include the following:

  • Aspiration of urine from the fetal bladder
  • Antenatal screening for aneuploidy - Chorionic villus sampling; amniocentesis; sampling maternal blood (not standardized)


Medical Care

At present, no medical interventions are indicated for the treatment of antenatal hydronephrosis (urinary tract dilation). However, medical therapy is indicated in fetuses with oligohydramnios and the resultant pulmonary hypoplasia.

Pulmonary hypoplasia is the precursor for bronchopulmonary dysplasia that develops in the neonate and is the major cause of mortality in this patient population. Surfactant is needed to decrease surface tension at the air-liquid interface of the alveoli, and glucocorticoids administered to the mother in the antepartum period have been shown to stimulate production of surfactant-associated proteins and enhance lung maturation.[43]

A number of randomized trials concluded that antenatal corticosteroids, given between 48 hours and 7 days before preterm delivery, decrease the incidence of respiratory distress syndrome and death.[44, 45] However, short-term adverse effects were noted, including hypertension, hyperglycemia, infections, intestinal perforations, gastrointestinal (GI) bleeding, inhibition of somatic growth, and hypertrophic cardiomyopathy.[46, 47, 48]  Potential long-term adverse effects included impaired somatic, lung, and brain growth.[43] Risks and benefits must be carefully weighed in each patient.

Surgical Care

Intervention for a fetus with antenatal hydronephrosis (dilatation of the upper urinary tract) is controversial for the following reasons:

  • Obtaining an accurate diagnosis with current technology is difficult
  • The natural history of each disease process causing antenatal hydronephrosis is variable and has not been fully elucidated
  • The lack of data regarding the success and complications of intervention has impeded progress in defining specific indications for treatment

The main considerations in evaluating a fetus with antenatal hydronephrosis are gestational age, laterality of the lesion, the presence of unfavorable prognostic factors, volume of amniotic fluid, and overall fetal well-being.

Lesions detected early in fetal development may have a significant impact on renal and pulmonary development. Laterality of the lesion is significant, with bilateral lesions being more predictive of poor outcome. The presence of unfavorable prognostic factors, such as renal cortical cysts and echogenic parenchyma on antenatal ultrasonography (US), elevated levels of urinary electrolytes on vesicocentesis, and reduced lung volume or thoracic circumference, should also be considered.[49]

The presence of oligohydramnios is the most significant indicator of poor fetal outcome, and intervention should not be considered in its absence. In the presence of multiple fetal anomalies or chromosomal anomalies predictive of poor outcome, parents may elect to terminate the pregnancy.

A management strategy has been developed on the basis of findings from initial and serial antenatal US.[28] Significant unilateral hydronephrosis does not necessitate antenatal intervention; however, it should be evaluated in the postnatal period with follow-up renal US (if needed), voiding cystourethrography (VCUG), and diuretic renography.[50, 51]

Bilateral hydronephrosis without bladder distention is more significant and should be monitored ante partum with serial US examinations to look for bladder distention and development of oligohydramnios. Postnatal evaluation should be performed as above. A fetus that presents with bilateral hydronephrosis and a distended bladder should raise serious concern for an obstructive process, such as urethral atresia or urethral valves.

If oligohydramnios is not present, serial examinations are adequate with definite postnatal evaluation as described above. In the presence of oligohydramnios, evaluation for the presence of unfavorable prognostic factors with karyotype analysis and vesicocentesis is warranted. Referral to a tertiary care center should also be a consideration. Fetuses with findings consistent with a poor outcome generally are not good candidates for antenatal intervention. Personnel and technology should be available to perform the necessary workup and offer intervention if this course of action is deemed appropriate.

Fetuses whose antenatal hydronephrosis is milder (but still suggestive of a significant underlying pathologic cause) require immediate neonatal consultation with a pediatric urologist. This consultation can direct further inpatient workup or provide an outlet for outpatient monitoring.

Treating a potentially obstructive process in the presence of oligohydramnios by diversion of urine into the amniotic space would seemingly allow normal renal and lung development. Relief of the obstructed flow of urine should optimize eventual renal function, and restoration of normal levels of amniotic fluid should prevent the development of pulmonary hypoplasia. However, both experimentally and in clinical situations, this is not entirely true.

Sufficient evidence indicates that restoring amniotic fluid volume is beneficial for lung development and preventing pulmonary hypoplasia; however, little evidence indicates that renal function is improved with this intervention. Experimental models and autopsy evaluations have demonstrated that irreversible dysplasia is often present by the time hydronephrosis is detected.[28] Intervention should only be considered in fetuses with oligohydramnios and a significant chance of recovery of renal function on the basis of renal prognostic factors.

Antenatal intervention is limited by technical considerations and lack of adequate comparison between the varying modalities with regard to patient selection and outcome measures, especially whether fetal intervention improves postnatal outcomes. Numerous advances have been made in refining current modalities; however, no prospective randomized trials are currently under way that compare the outcomes of the various interventions.

The first successful in-utero decompression was achieved with open fetal surgery by creating bilateral cutaneous ureterostomies in a 21-week fetus.[52] Although the intervention was successful, the neonate did not survive, because of pulmonary complications.

Open vesicostomies have also been attempted; however, these open interventions have been abandoned in favor of percutaneous shunt procedures.

Such approaches were eloquently described in a review by Freedman et al, who discussed several technical advances that allowed more success than was achieved in initial attempts (eg, use of amnioinfusion to enhance fetal visualization, use of fetal paralysis, routine use of antibiotics, and increased focus on proper catheter placement), as well as specific outcome measures needed for appropriate evaluation of the effects of fetal intervention (eg, gross survival, postnatal survival, shunted survival, and nadir creatinine at 1 year).[4]

Laparoscopic approaches have also been described[53, 54]  but have been associated with high rates of complications.

Fetal cystoscopic ablation of posterior urethral valves has been described; success rates have varied.[55] The fetoscope is passed percutaneously through a cannula into the fetal bladder, and ablation of the valves is achieved with laser coagulation.

Other less invasive techniques have been developed to help prevent oligohydramnios-induced pulmonary hypoplasia. As previously mentioned, serial transabdominal amnioinfusion is helpful in placement of percutaneous shunts. It may also have a therapeutic role in the reduction of pulmonary hypoplasia.[56] This intervention could be useful in fetuses with oligohydramnios associated with antenatal hydronephrosis.


Consultations are indicated as directed by the initial evaluation but may include the following:

  • Neonatologist
  • Pediatrician
  • Pediatric urologist
  • Pediatric nephrologist
  • Pediatric cardiologist
  • Pediatric cardiac surgeon
  • Pediatric surgeon
  • Pediatric orthopedic surgeon
  • Pediatric neurosurgeon

Long-Term Monitoring

Most neonates with antenatal hydronephrosis (dilatation of the upper urinary tract) can be discharged home, provided that inpatient evaluation does not preclude further evaluation or intervention in a hospital setting. Djahangirian et al suggested that whereas patients with an initial postnatal APD of 10 mm or greater and a SFU grade of 3-4 should be followed, all patients with an APD of less than 10 mm, especially with an SFU grade of 1-2, can be safely discharged, in that they are unlikely to experience complications.[57]

Outpatient follow-up with the pediatric urologist depends on the diagnosis (see DDx). Evaluation and management of the neonate or infant in the outpatient setting is directed by the underlying cause of antenatal and postnatal hydronephrosis. Appropriate follow-up with other subspecialties may also be necessary if antenatal and postnatal evaluation warrants such management.

Typically, neonates with antenatal hydronephrosis are evaluated with postnatal US. The optimal timing of the initial postnatal US examination is not important, provided that repeat serial imaging is done so as to ensure that the degree of hydronephrosis in a relatively dehydrated neonate is not underestimated.[58]  Postnatal US 1-4 weeks after birth is recommended.

The most common inpatient and/or outpatient medication prescribed in the setting of antenatally detected hydronephrosis persisting in the postnatal period is a prophylactic antibiotic against urinary tract infection (UTI). This medication is given with the aim of preventing UTIs and possible renal damage that may result from pyelonephritis. It is not prescribed to all patients with hydronephrosis and is administered to patients according to the underlying cause of their hydronephrosis. Generally, a penicillin-based antibiotic is appropriate in this age group.

Herz et al studied 405 children with asymptomatic antenatal hydronephrosis, of whom 278 received continuous antibiotic prophylaxis (CAP) and 178 did not.[59]  They concluded that CAP may have a significant role to play in reducing the risk of febrile UTI for children with identifiable risk factors (eg, ureteral dilatation, high-grade vesicoureteral reflux, and ureterovesical junction obstruction) but appears to be unnecessary otherwise.

The European Association of Urology/European Society for Paediatric Urology Guidelines Panel carried out a systematic review aimed at determining whether CAP is effective for antenatal hydronephrosis and, if so, what the most and least beneficial antibiotic regimens are.[60] ​ Outcomes included reduced UTIs, decreased drug-related adverse events (AEs), and improved kidney function. The Panel was unable to establish whether CAP is superior to observation in decreasing UTIs, nor could it reach any conclusions about drug-related AEs or kidney function, because of lack of data. There was some evidence that CAP can reduce febrile UTI in particular subgroups.




Class Summary

These agents elicit anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.

Betamethasone (Celestone Soluspan)

Prenatal betamethasone is administered to pregnant women according to the recommendations by a National Institutes of Health (NIH) Consensus Conference Panel for all pregnancies at 24-34 weeks' gestation at risk of preterm delivery, preterm premature rupture of membranes (PROM) at 30-32 weeks' gestation, and in complicated pregnancies with anticipated delivery at < 34 weeks' gestation. Reduces neonatal mortality rates, respiratory distress syndrome (RDS), and intraventricular hemorrhage (IVH).


Class Summary

Exogenous surfactant can be helpful in treatment of airspace disease (eg, RDS). Following inhaled administration, surface tension is reduced and alveoli are stabilized, thus decreasing the work of breathing and increasing lung compliance.

Beractant (Survanta)

A semisynthetic bovine lung extract containing phospholipids, fatty acids, and surfactant-associated proteins B (7 mcg/mL) and C (203 mcg/mL).

Calfactant (Infasurf)

A natural calf lung extract containing phospholipids, fatty acids, and surfactant-associated proteins B (260 mcg/mL) and C (390 mcg/mL).