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Pediatrics: Surgery > Urology
Antenatal Hydronephrosis
Article Last Updated: May 25, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 10
Author: Dennis B Liu, MD, Pediatric Urology Fellow, Children's Memorial Hospital in Chicago, Northwestern University Feinberg School of Medicine
Dennis B Liu is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Urologists, American College of Surgeons, American Urological Association, and Endourological Society
Coauthor(s):
John D Edmondson, MD, Consulting Staff, Virginia Urology Center
Editors: Martin David Bomalaski, MD, FAAP, Pediatric Urologist, Alaska Southcentral Urology Specialists; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Harry P Koo, MD, Chairman of Urology Division and Director of Pediatric Urology, Virginia Commonwealth University; Professor of Surgery, VCU School of Medicine, Medical College of Virginia; Director of Urology, Children's Hospital of Richmond; Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System; William J Cromie, MD, MBA, President and Chief Executive Officer, Health Care, Capital District Physicians' Health Plan
Author and Editor Disclosure
Synonyms and related keywords:
antenatal hydronephrosis, congenital hydronephrosis, fetal hydronephrosis, urinary tract, ultrasonography, ultrasound, oligohydramnios
Background
This article focuses on hydronephrosis that is detected by prenatal ultrasonography. 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 (Elder, 1997; Johnson, 1992; Saari-Keppainen, 1990). If not for prenatal ultrasonographic detection, many of these urologic anomalies would manifest later in life as pyelonephritis, symptomatic flank or abdominal pain, renal calculi, hypertension, or even renal failure.
Degree and laterality of hydronephrosis are dependent on the stage of pregnancy and the underlying etiology. Ultrasonography can detect the fetal bladder and kidney by 15 weeks' gestation and distinguish a central echo (renal sinus) by 18-20 weeks' gestation (Johnson, 1992). At 20 weeks' gestation, the fetus is larger and an anomaly is easier to detect. Antenatal hydronephrosis has received significant attention since prenatal ultrasonography became a mainstream screening tool, yet it remains a controversial topic. Much of the controversy revolves around diagnosis and management.
Diagnostic dilemmas involve determining 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 causing a significant threat of neonatal death due to pulmonary hypoplasia are considered candidates for antenatal treatment. Once prenatal treatment is decided upon, controversy remains regarding the efficacy of a therapeutic intervention because of the limited knowledge of the underlying natural history and the difficulty in standardizing patient selection and determining appropriate outcome measures (Freedman, 2000).
Pathophysiology
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 (Potter, 1972). 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 by 10 and 12 weeks' gestation, respectively. Current technology does not allow renal imaging prior to completion of nephrogenesis.
The placenta, not the fetal kidneys, functions as the fetal hemodialyzer maintaining salt and water homeostasis; however, the fetal kidney does begin producing hypotonic urine between the fifth and ninth weeks of gestation and increases throughout gestation to reach rates as high as 50 mL/h (Elder, 1997). 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. This obstructive process may not be pathologic but, instead, the result of normal development; however, if significant obstruction is present and persistent, nephrogenic tissue can be affected, resulting in varying degrees of cystic dysplasia and renal impairment (Bernstein, 1976).
Most anomalies of the urinary tract discovered in the prenatal period are characterized by hydronephrosis. Intuitively, these lesions may be considered obstructive in nature; however, antenatal hydronephrosis can be the result of nonobstructive processes, such as vesicoureteral reflux, 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.
Chronic partial unilateral ureteral obstruction has been experimentally demonstrated to result in significant renal damage, and early relief of the obstructive process is followed by significant hemodynamic recovery (Chevalier, 1996; Chevalier, 1988). 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. Other studies have not been as supportive of early correction of the obstructive process. Josephson noted that obstruction is associated with decreased renal blood flow, glomerular filtration, and potassium excretion, and only a small percentage of this damage is benefited by early intervention (Josephson, 1991).
Frequency
United States
Hydronephrosis is the most common pathologic finding in the urinary tract on prenatal screening by ultrasonography, accounting for 50% of all abnormal findings. The incidence varies among series because of criteria for dilation and timing of ultrasonography; however, the incidence of a significant uropathy in association with hydronephrosis is 0.2% (Thomas, 1990). International studies have supported this finding, with an incidence of 0.25% in Sweden and 0.92% in Great Britain.
Mortality/Morbidity
- Determination of mortality is difficult with antenatal hydronephrosis because of the significant incidence of stillbirths, terminated pregnancies, and missed diagnoses—all which lead to underestimation of true mortality rates. 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 (Madarikan, 1988; Ransley, 1985). In the presence of a bilateral obstructive process, oligohydramnios is the best predictor of an adverse outcome (Reznick, 1989; Hobbins, 1984). 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.
- The timing of oligohydramnios is an important determinant of fetal outcome. The earlier a lesion develops, the more likely it is to have an effect on the fetal kidney, lungs, and overall outcome of the fetus. In a series of 113 cases detected in the third trimester, the mortality rate was 13% (Bastide, 1986). Detection in the second trimester was almost uniformly fatal, with an 83-100% mortality rate (Barss, 1984). The most vulnerable period for pulmonary development is the second trimester; no adverse pulmonary effects from late-onset oligohydramnios occur (Wigglesworth, 1982; Mandell, 1992). In general, the major determinant of survival is pulmonary development.
Race
No known studies report the incidence of antenatal hydronephrosis related to race.
Sex
The incidence of antenatal hydronephrosis related to sex has not been reported.
Age
Studies have uniformly shown that timing of hydronephrosis is important. Early onset of hydronephrosis in fetal development is directly related to prognosis.
History
- The finding of antenatal hydronephrosis should prompt a series of inquires in regards to onset, fetal sex, oligohydramnios, laterality, severity of hydronephrosis, bladder cycling, other anomalies, prior pregnancy complications, and family history of urologic disease.
- Ultrasonographic evaluation can provide important information, such as sex of the fetus, unilateral or bilateral disease, renal anterior-posterior (AP) pelvic diameter, bladder distension, bladder sagittal length, volume of amniotic fluid, and associated pathologic conditions. For example, Reuss et al found that 16 of 31 (55%) fetuses with bilateral hydronephrosis and oligohydramnios had an associated structural or chromosomal abnormality (Reuss, 1988).
- Other aspects of the history that can be helpful in identifying the cause of hydronephrosis include family and maternal history.
Physical
See History.
Causes
A number of pathologic entities can cause antenatal hydronephrosis. 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. As reviewed in 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 hydronephrosis. Once canalization is complete, this obstruction is relieved, and hydronephrosis should resolve. The goal of evaluation is to differentiate benign physiologic dilation from significant obstructive disease or reflux.
Genital Anomalies
Meatal Stenosis
Posterior Urethral Valves
Radiographic Evaluation of the Pediatric Urinary Tract
Ureteropelvic Junction Obstruction
Vesicoureteral Reflux
Other Problems to be Considered
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
Lab Studies
Imaging Studies
- Prenatal ultrasonography is the imaging modality that originally brought the patient with antenatal hydronephrosis to medical attention. This is the main means of radiographically evaluating and monitoring the fetus. Antenatal ultrasonographic detection of fetal genitourinary abnormalities first was reported in 1970 (Garrett, 1970). Since that time, assessment of the genitourinary system is routine and should be part of every fetal ultrasonographic examination. If an abnormality is found on the screening or dating ultrasound, 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 (Coplen, 2000). Prenatal ultrasonography 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.
- 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 (Johnson, 1992; Stocks, 1996).
- Renal AP pelvic diameter is used to evaluate the significance of dilation. In one series, 94% of fetuses with a renal AP diameter of greater than 2 cm, 50% with an AP diameter of 1-1.5 cm, and only 3% with an AP diameter of less than 1 cm required surgery or at least long-term monitoring for a significant urinary tract lesion (Grignon, 1986). More recently, a renal AP pelvic diameter of at least 4 mm before 33 weeks' gestation and at least 7 mm after 33 weeks' gestation is considered significant (Corteville, 1991). Caliectasis correlates best with the presence of a significant dilation or an obstructive process.
- 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 (Coplen, 2000).
- 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 (Maizels, 2004).
- Renal architecture, renal size, and echogenicity of the renal parenchyma are important in developing a differential and determining the potential function of the kidney.
- Caliceal anatomy revealed by ultrasonography 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 (Dewan, 2002).
- 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 calyces and pelvis. Polycystic kidneys do not appear as orderly, and connections between cysts are not present.
- Renal size and echogenicity also are 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(s). These findings are nearly 100% specific but accurately predict dysplasia in only 60% of fetuses (Crombleholme, 1990).
- 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. 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 (Reuss, 1988). These anomalies are commonly of cardiovascular, neurologic, and orthopedic origin, but they can be found elsewhere and should be sought during the imaging evaluation.
Other Tests
- Chromosomal analysis
- 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 ultrasonographic examination reduce the risk of a chromosomal abnormality 2- to 3-fold compared with fetuses having minor and major abnormalities on ultrasonography (Biedermann, 2001).
- Maternal serum biochemistries, such as beta–human chorionic gonadotropin (b-hCG), alpha-fetoprotein, and others, are used to detect aneuploidy, with reported accuracy of approximately 65%. The best individual risk estimation is based on maternal age, ultrasonographic examination, and maternal biochemistry (Biedermann, 2001).
- 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.
- Recent 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 (Parano, 2001). Although promising, these techniques are not standardized or available to the population at large.
Procedures
- Aspiration of urine from the fetal bladder
- Prenatal screening for aneuploidy
- Chorionic villus sampling
- Amniocentesis
- Sampling maternal blood (not standardized)
Medical Care
- To date, no medical interventions for the treatment of antenatal hydronephrosis exist. However, medical therapy is indicated in fetuses with oligohydramnios and the resultant pulmonary hypoplasia. Pulmonary hypoplasia is the precursor for bronchopulmonary dysplasia (BPD) 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 prenatal period have been shown to stimulate production of surfactant-associated proteins and enhance lung maturation (Bolt, 2000).
- Randomized trials have concluded that antenatal corticosteroids, administered between 48 hours and 7 days before preterm delivery, decrease the incidence of respiratory distress syndrome and death (Crowley, 1972; Crowley, 2000). However, short-term adverse effects include hypertension, hyperglycemia, infections, intestinal perforations, gastrointestinal bleeding, inhibition of somatic growth, and hypertrophic cardiomyopathy (Halliday, Cochrane Database Syst Rev, 2000; 2: CD001146; Halliday, Cochrane Database Syst Rev, 2000; 2: CD001144; Halliday, 2001). Long-term adverse effects may include impairment of somatic, lung, and brain growth (Bolt, 2000). Risks and benefits must be carefully weighed in each patient.
Surgical Care
- Intervention for a fetus with antenatal hydronephrosis is controversial for a variety of reasons. First, obtaining an accurate diagnosis with current technology is difficult. Second, the natural history of each disease process causing antenatal hydronephrosis is variable and has not been fully elucidated. Finally, 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 prenatal ultrasonography, elevated levels of urinary electrolytes on vesicocentesis, and reduced lung volume or thoracic circumference, should also be considered (Yoshimura, 1996). 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 based on initial and serial prenatal ultrasonographic findings (Coplen, 2000). Significant unilateral hydronephrosis does not require prenatal intervention; however, it should be evaluated in the postnatal period with follow-up renal ultrasonography and voiding cystourethrography.
- Bilateral hydronephrosis without bladder distension is more significant and should be monitored prenatally with serial ultrasonographic examinations to monitor for bladder distension 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 are generally not good candidates for prenatal intervention.
- Intuitively, 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, 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 (Coplen, 1997). Intervention should only be considered in fetuses with oligohydramnios and a significant chance of recovery of renal function based on renal prognostic factors.
- Prenatal 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 currently exist comparing 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 (Harrison, 1982). 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. An eloquent description can be found in a review by Freedman et al (Freedman, 2000). They describe several advances in technique that have allowed more success than in initial attempts, such as use of amnioinfusion to enhance fetal visualization, use of fetal paralysis, routine use of antibiotics, and increased appreciation of proper catheter placement. They also describe specific outcome measures that are needed for appropriate evaluation of the effects of fetal intervention, including gross survival, postnatal survival, shunted survival, and nadir creatinine at 1 year.
- Fetal cystoscopic ablation of posterior urethral valves has been described with varying success (Quintero, 1995). 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 alluded to above, serial transabdominal amnioinfusion is helpful in placement of percutaneous shunts. It may also have a therapeutic role in the reduction of pulmonary hypoplasia (Vergani, 1997). This intervention could be useful in fetuses with oligohydramnios associated with antenatal hydronephrosis.
Consultations
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
Drug Category: Glucocorticoids
These agents elicit anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.
| Drug Name | Betamethasone (Celestone, Soluspan) |
| Description | 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). |
| Adult Dose | 12 mg IM qd for 2 doses (repeated courses optional but associated with significant adverse effects) |
| Contraindications | PROM <29 weeks' gestation; diabetes mellitus; gestational diabetes mellitus; severe preeclampsia |
| Interactions | Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; betamethasone decreases effect of salicylates and vaccines used for immunization |
| Pregnancy | C - Safety for use during pregnancy has not been established.
|
| Precautions | Multiple courses of antenatal betamethasone produce higher frequency of early-onset neonatal sepsis, chorioamnionitis, endometritis, and neonatal death; case reports of transient hypertrophic cardiomyopathy and cushingoid syndrome in neonates |
Drug Category: Surfactants
Exogenous surfactant can be helpful in treatment of airspace disease (eg, respiratory distress syndrome). Following inhaled administration, surface tension is reduced and alveoli are stabilized, thus decreasing the work of breathing and increasing lung compliance.
| Drug Name | Beractant (Survanta) |
| Description | A semisynthetic bovine lung extract containing phospholipids, fatty acids, and surfactant-associated proteins B (7 mcg/mL) and C (203 mcg/mL). |
| Pediatric Dose | 100 mg (ie, 4 mL)/kg intratracheally divided in 4 aliquots administered at least 6 h apart |
| Contraindications | None known |
| Interactions | None reported |
| Pregnancy | |
| Precautions | Must be warmed to room temperature; administer only under carefully supervised conditions because of risk of acute airway obstruction |
| Drug Name | Calfactant (Infasurf) |
| Description | A natural calf lung extract containing phospholipids, fatty acids, and surfactant-associated proteins B (260 mcg/mL) and C (390 mcg/mL). |
| Pediatric Dose | 3 mL/kg intratracheally; may repeat q6-12h; not to exceed 3-4 doses |
| Contraindications | None known |
| Interactions | None reported |
| Pregnancy | |
| Precautions | Administer only under carefully supervised conditions because of risk of acute airway obstruction |
Further Inpatient Care
- A detailed description of situations requiring further inpatient care is provided in Surgical Care. Briefly, fetuses with bilateral hydronephrosis, a distended bladder, and oligohydramnios require further evaluation in a tertiary care center. Personnel and technology should be available to perform the necessary workup and offer intervention if this course of action is deemed appropriate. Fetuses with milder forms of antenatal hydronephrosis (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.
Further Outpatient Care
- Most neonates with antenatal hydronephrosis can be discharged to home provided that the inpatient evaluation does not preclude further evaluation or intervention in a hospital setting. Outpatient follow-up with the pediatric urologist depends on the diagnosis, which is summarized in Differentials. Evaluation and management of the neonate or infant in the outpatient setting is directed by the underlying cause of antenatal and postnatal hydronephrosis. Arranging appropriate follow-up with other subspecialties may also be necessary if the prenatal and postnatal evaluation warrants this type of management.
In/Out Patient Meds
- 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. This medication is required to prevent urinary tract infections and possible renal damage. This medication is not prescribed to all patients with hydronephrosis and is administered to patients based on the underlying cause of their hydronephrosis. Generally, a penicillin-based antibiotic is appropriate in this age group.
Complications
- Fetuses at highest risk of 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.
Prognosis
- Most neonates with antenatal hydronephrosis have an excellent prognosis. Prognosis is largely dependent on the underlying etiology of the dilated collecting system. Severe bilateral hydronephrosis that is associated with obstruction and oligohydramnios detected early in gestation is the best predictor of an adverse outcome.
Patient Education
- Many fetuses have an excellent prognosis, and this should be communicated to the parents. If a fetus has ultrasonographic findings suggestive of an adverse outcome, discussing the implications and providing the parents with information regarding further evaluation and management of their pregnancy is important.
Medical/Legal Pitfalls
- Antenatal hydronephrosis is caused by physiologic and pathologic conditions that may or may not warrant close medical attention. The practitioner must make the appropriate decisions regarding evaluation and treatment of these underlying conditions. The medical field is well aware of the legal ramifications of missed diagnoses that result in harmful outcomes for patients, and this condition is no different.
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Antenatal Hydronephrosis excerpt Article Last Updated: May 25, 2006
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