Problem. Urine output has been scant or absent for 24 h. Oliguria is defined as urine output <0.5–1 mL/kg/h. One hundred percent of healthy premature, full-term, and postterm infants void by 24 h of age. Oliguria is one of the clinical hallmarks of renal failure.
Is the bladder palpable? If a distended bladder is present, it is usually palpable. A palpable bladder suggests there is urine in the bladder. Credé maneuver (manual compression of the bladder) may initiate voiding, especially in infants receiving medications causing muscle paralysis.
Has bladder catheterization been performed? Catheterization determines whether urine is present in the bladder. It is commonly done in more mature infants.
What is the blood pressure? Hypotension can cause decreased renal perfusion and urine output.
Has the infant ever voided? If the infant has never voided, consider bilateral renal agenesis, renovascular accident, or obstruction. Table 61–1 shows the time after birth at which the first voiding occurs.
Did the mother have oligohydramnios? One of the etiologies of oligohydramnios, a decrease in amniotic fluid, can be caused by a decrease in fetal urine production. This can be caused by fetal renal problems such as decreased renal perfusion, obstructive uropathy, and congenital absence of renal tissue (renal agenesis, cystic dysplasia, and ureteral atresia).
Differential diagnosis. For a complete discussion of acute renal failure, see Chapter 113.
Prerenal causes (normal kidneys with inadequate renal perfusion)
Sepsis/Shock. Renal failure occurs in 26% of neonates with sepsis.
Asphyxia. Sixty-one percent of infants with asphyxia have renal failure, 25% of cases are oliguric, and 15% are anuric.
Medications. Certain medications (eg, indomethacin, captopril, and β-agonists), if given to the mother before delivery, can result in renal insufficiency.
Respiratory distress syndrome.
Intrinsic renal failure (structural renal damage)
Hypoplastic, dysplastic, or polycystic kidneys.
Vascular accident (renal artery and vein thrombosis).
Infections such as congenital syphilis, cytomegalovirus, toxoplasmosis, and Gram-negative infections.
Acute tubular necrosis secondary to shock, dehydration, drugs, toxins, and asphyxia.
Medications. Some nephrotoxic medications include tolazoline, aminoglycosides, indomethacin, amphotericin, α-adrenergic agents, nonsteroidal anti-inflammatory drugs, diuretics, and acyclovir.
Postrenal causes (urine is formed but not passed)
Neurogenic bladder (from myelomeningocele or medications such as pancuronium or heavy sedation).
Posterior urethral valves (males only).
Extrinsic compression (eg, sacrococcygeal teratoma).
Drugs. Certain medications (eg, acyclovir and sulfonamides) can precipitate within the tubules and cause obstruction.
Systemic candidiasis with bilateral uteropelvic fungal bezoar formation.
Physical examination may reveal bladder distention, abdominal masses, or ascites. Signs of renal disorders (eg, Potter facies [low-set ears, inner canthal crease, etc.]) should be noted. Urinary ascites may be seen with posterior urethral valves. Oligohydramnios in the mother suggests possible renal problems.
Prerenal. Signs of volume depletion (tachycardia and hypotension).
Intrinsic renal. Edema, signs of congestive heart failure, hypertension. Palpable kidneys may mean polycystic kidney, hydronephrosis, or tumors.
Postrenal. Poor urinary stream, enlarged bladder, and dribbling of urine; urinary ascites with rupture.
Laboratory studies. The following laboratory tests can be obtained to help establish the diagnosis. Interpret the results as outlined in Table 113–1.
Serum electrolytes and blood urea nitrogen also help to ...
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