I have not urinated in 24 hours

Asked by: Ben Warwick, Poole

The bladder holds 400-600ml of urine. Normal urine production is around 1.5 litres every 24 hours, so that would give you nine or 10 hours to completely fill up.

However you can drop to as little as 400ml of urine production a day for short periods without suffering harmful consequences. This could conceivably give you as long as 36 hours between trips to the loo.

Read more:

• Do birds urinate?
• Is there really poo everywhere?

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Authors

Luis trained as a zoologist, but now works as a science and technology educator. In his spare time he builds 3D-printed robots, in the hope that he will be spared when the revolution inevitably comes.

Urine output has been scant or absent for 24 hours. One hundred percent of healthy premature, full-term, and post-term infants void by 24 hours of age. Oliguria is defined as urine output <1.0 mL/kg/h for 24 hours. Anuria is defined as absence of urine output usually by 48 hours of age. Oliguria is one of the clinical hallmarks of renal failure. Decreased urine output can be from mild dehydration or acute renal failure (ARF) or acute kidney injury (AKI). ARF/AKI is an acute renal dysfunction and occurs when there is a decrease in glomerular filtration rate, an increase in creatinine and nitrogenous waste products with the loss of ability to regulate fluid and electrolytes. Incidence of neonatal ARF/AKI is around 6–24%. There is a high percentage of ARF/AKI in very low birthweight infants, infants postcongenital heart surgery, infants on extracorporeal membrane oxygenation/extracorporeal life support (ECMO/ECLS) (especially with a congenital diaphragmatic hernia), and infants with perinatal depression.

1. 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.

2. Has bladder catheterization been performed? Catheterization determines whether urine is presentin the bladder. It is commonly done in more mature infants.

3. What is the blood pressure? Hypotension can cause decreased renal perfusion and urine output. Hypertension may indicate renal/renovascular disease (if severe, suspect renal artery or venous thrombosis).

4. Has the infant ever voided? Did the infant void and was it not recorded on the bedside chart? If the infant has never voided, consider bilateral renal agenesis, renovascular accident, or obstruction. Table 68–1 shows the time after birth at which the first voiding occurs. Remember: voiding can be missed (occurred in the delivery room or with the parents and was not recorded). Approximately 13–21% of infants void in the delivery room.

5. Did the mother have oligohydramnios? One of the etiologies of oligohydramnios (decrease in amniotic fluid) can be caused by a decrease in fetal urine production. This can be caused by renal problems such as decreased renal perfusion, obstructive uropathy, and congenital absence of renal tissue (renal agenesis, cystic dysplasia, and ureteral atresia).

6. Is there gross hematuria? Gross hematuria suggests intrinsic renal disease.

7. What medications was the mother on during her pregnancy? Certain medications (eg, angiotensin-converting enzyme [ACE] inhibitors, nonsteroidal anti-inflammatory drugs [NSAIDS]), if given to the mother during her pregnancy, may interfere with fetal nephrogenesis which can result in fetal renal injury and lead to acute kidney injury in the newborn. ACE inhibitors during pregnancy can cause renal tubular dysgenesis in the infant.

8. Does the infant have a congenital renal disease? Did the prenatal ultrasound suggest kidney disease? Acute renal failure in the newborn may have a prenatal onset. Renal agenesis, renal dysplasia, polycystic kidney disease, and congenital nephrotic syndrome, or any obstruction can all cause acute renal failure in the newborn.

9. Did the mother have diabetes? Infants of diabetic mothers have an increased risk of renal anomalies (renal agenesis, hydronephrosis, and ureteral duplication).

Table 68–1.TIME OF FIRST VOID BASED ON A STUDY OF 500 TERM AND PRETERM INFANTS

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Table 68–1.TIME OF FIRST VOID BASED ON A STUDY OF 500 TERM AND PRETERM INFANTS

A delay in urination can be from mild dehydration or ARF/AKI. For a complete discussion of ARF/AKI, see Chapter 123.

1. Mild dehydration. An infant may have decreased urination the first couple of days of life, especially if the infant is breast-feeding. Inadequate breast milk production can cause dehydration. Laboratory findings are usually normal or may show a minimal change.

2. Acute renal failure/acute kidney injury. Definitions vary and can be based on serum creatinine (see Section IV.C.1). ARF/AKI can be caused by prerenal, renal, and postrenal causes.

   1. Prerenal failure (most common type). Normal kidneys with inadequate or decreased renal blood flow (perfusion). This leads to decreased renal function. Renal hypoperfusion can be caused by a true volume depletion (hemorrhage, dehydration, third space losses) or a decreased effective blood volume (a disease process that results in decreased perfusion to the kidney such as congestive heart failure or cardiac tamponade). Common causes in the neonatal intensive care unit (NICU) are

      1. Hemorrhage (perinatal or postnatal).

      2. Dehydration.

      3. Sepsis. Renal failure occurs in 26% of neonates with septic shock.

      4. Necrotizing enterocolitis.

      5. Respiratory distress syndrome.

      6. Shock and hypotension.

      7. Gastrointestinal losses.

      8. Third space losses.

      9. Cardiac. Congestive heart failure, patent ductus arteriosus, congenital heart disease/cardiac surgery, pericarditis, cardiac tamponade.

      10. Polycythemia can cause a decrease in GFR, oliguria, hematuria, and renal vein thrombosis.

      11. Infants requiring ECMO/ECLS can experience fluid overload and decreased renal blood flow.

      12. Hypoalbuminemia.

      13. Medications. Any medications that can decrease renal blood flow can lead to prerenal disease. These include indomethacin, NSAIDS, aminoglycosides, amphotericin, adrenergic drugs (phenylephrine eye drops), and ACE inhibitors (captopril).

   2. Intrinsic renal disease (kidney injury). This occurs due to structural renal damage to the tubules, glomeruli, or interstitium. Most often it is renal tubular dysfunction caused by an acute insult. Acute tubular necrosis (ischemic, drug, or toxin induced), glomerular lesions, and vascular lesions make up most of intrinsic renal failure.

      1. Acute tubular necrosis. Most common cause of intrinsic renal disease and can be secondary to shock, dehydration, toxins, perinatal asphyxia, cardiac surgery, ischemic or hypoxic insults, drug induced or IV contrast media. Perinatal asphyxia is the most common cause of acute tubular necrosis. There is a large percentage of infants with severe perinatal asphyxia who have renal failure (25% of cases are oliguric and 15% are anuric). Prolonged prerenal failure that is not treated will progress to acute tubular necrosis.

      2. Interstitial nephritis. Either drug induced or idiopathic.

      3. Congenital renal anomalies. Renal tubular dysgenesis, renal agenesis (Potter syndrome), polycystic kidney disease, congenital nephrotic syndrome, hypoplastic or dysplastic kidneys.

      4. Infections. Acute pyelonephritis, sepsis, gram-negative infections, candidiasis, and congenital infections (toxoplasmosis, cytomegalovirus, syphilis).

      5. Vascular lesions. Bilateral renal artery thrombosis or bilateral renal vein thrombosis. Ischemic or hypoxic insults (twin-to-twin transfusion, abruptio placentae, or perinatal asphyxia) can cause renal cortical necrosis.

      6. Nephrotoxic medications. Some nephrotoxic medications commonly used in the NICU include aminoglycosides, vancomycin, acyclovir, NSAIDS, IV contrast media, ACE inhibitors (eg, captopril, enalapril), and amphotericin B. Nephrotoxic ARF/AKI is usually associated with aminoglycoside antibiotics and NSAIDS that are used to close a patent ductus arteriosus. Diuretics may increase the nephrotoxicity of other medications (eg, NSAIDS).

      7. Endogenous toxins (rare). Uric acid (uric acid nephropathy), myoglobin, free hemoglobin.

   3. Postrenal causes. (Where urine is formed but not passed.) More common in newborn infants than older infants. Caused by a mechanical or functional obstruction to the flow of urine. The obstruction can be in the upper tract such as bilateral ureteropelvic junction obstruction or lower tract such as posterior urethral valves.

      1. Neurogenic bladder from myelomeningocele or medications such as pancuronium or heavy sedation.

      2. Obstruction for any reason in a solitary kidney.

      3. Meatal stenosis (usually males).

      4. Bilateral ureteral obstruction (bilateral ureteropelvic junction obstruction).

      5. Urethral stricture.

      6. Posterior urethral valves (males only) may also be complicated by bladder rupture.

      7. Extrinsic compression (eg, sacrococcygeal teratoma).

      8. Drugs. Certain medications (eg, acyclovir and sulfonamides) can precipitate within the tubules and cause obstruction.

      9. Systemic candidiasis with bilateral ureteropelvic fungal bezoar formation (fungal balls causing obstruction).

      10. Spontaneous rupture of the bladder with anuric renal insufficiency.

      11. Occult ureteropelvic junction obstruction presenting as anuria.

      12. Imperforate hymen (female) causing hydrometrocolpos, anuria, and bilateral hydronephrosis.

1. Prenatal and maternal history. Review for oligohydramnios, genetic renal disorders, list of maternal medications. Was there any risk of infection? Did bleeding occur during the delivery? Did perinatal asphyxia occur? Was there maternal hypovolemia?

2. Physical examination. First, determine the state of hydration. Is the infant dehydrated? Is there evidence of congestive heart failure? Is the infant edematous? Does the infant have hypertension/hypotension? Examination of the abdomen may reveal bladder distention (bladder outlet obstruction), abdominal masses, or ascites (ruptured obstructed urinary tract). Signs of renal disorders (eg, Potter facies [low-set ears, inner canthal crease]) should be noted. Dysmorphic features suggestive of renal disease include single umbilical artery, hypospadias, anorectal abnormalities, vertebral anomalies, abnormal ears, and esophageal atresia. Urinary ascites may be seen with posterior urethral valves. Oligohydramnios suggests possible renal problems.

   1. Prerenal. Signs of volume depletion (tachycardia and hypotension).

   2. Intrinsic renal. Edema, signs of congestive heart failure, hypertension. Palpable kidneys may mean polycystic kidney, hydronephrosis, or tumors.

   3. Postrenal. Poor urinary stream, enlarged bladder, and dribbling of urine; urinary ascites with rupture.

3. Laboratory studies. The following laboratory tests can help establish the diagnosis in cases of low urine output. Interpret the results as outlined in Table 123–1. Remember blood urea nitrogen (BUN) and creatinine levels will reflect maternal function shortly after birth.

   1. Serum creatinine is used to define ARF/AKI and multiple definitions exist.

      1. Persistent elevation of serum creatinine or a serum creatinine ≥1.5 mg/dL is diagnostic of acute renal failure (if maternal renal function normal).

      2. Definition and staging for ARF/AKI based on serum creatinine proposed by Jetton and Askenazi:

         1. No ARF/AKI. No change in serum creatinine or an increase <0.3 mg/dL from a previous trough level.

         2. Stage 1 ARF/AKI. An increase in serum creatinine of 0.3 mg/dL or 1.5 to 2 times from the previous trough level.

         3. Stage 2 ARF/AKI. An increase in the serum creatinine by 2 to 3 times from the previous trough level.

         4. Stage 3 AFR/AKI. A serum creatinine ≥ 2.5 mg/dL, or a 3 times increase from the previous trough level, or the need for dialysis.

   2. Serum electrolytes and blood urea nitrogen also help to evaluate renal function. An increased BUN and BUN/serum creatinine >20 are seen in prerenal oliguria. BUN/creatinine ratio of 10–15 can be seen in intrinsic renal damage. Electrolytes can be abnormal, especially potassium (hyperkalemia) with renal failure.

   3. Complete blood and platelet count. An abnormal complete blood count can be seen in sepsis. Thrombocytopenia or polycythemia can be seen in bilateral renal vein thrombosis.

   4. Urinalysis. Most likely normal in prerenal disease and urinary tract obstruction. May reveal white blood cells, suggesting a urinary tract infection. Red blood cells, tubular cells, and proteinuria suggest intrinsic renal disease. Erythrocyte casts are seen in glomerulonephritis. Protein in the urine can indicate glomerular disease. Epithelial casts and brown granular casts can be seen in acute tubular necrosis.

   5. Arterial blood pH. A metabolic acidosis can be seen in anything that causes hypovolemia, hypoperfusion, or hypotension, such as sepsis.

   6. Urinary indices. See Table 123–1. Osmolality, urine sodium, urine-to-plasma creatinine ratio, fractional excretion of sodium, and renal failure index can help in the evaluation of deciding if the renal failure is prerenal or intrinsic.

   7. Urinary neutrophil gelatinase-associated lipocalin levels at birth. May be able to predict renal function earlier than serum creatinine in very low birthweight infants.

4. Imaging and other studies

   1. Renal ultrasonography with Doppler flow studies of the abdomen and kidneys will rule out urinary tract obstruction and help evaluate for other renal, congenital disorder, or vascular abnormalities. Doppler examination of renal blood flow can diagnose renal vascular thrombosis.

   2. Abdominal radiograph studies may reveal ascites or masses. Spina bifida or an absent sacrum suggests neurogenic bladder.

   3. Voiding cystourethrography can help diagnose lesions of the lower tract that cause obstruction if bladder outlet obstruction is suspected. It can also rule out vesicoureteral reflux.

   4. Radionuclide renal scanning may be helpful in obstruction.

For management of renal failure, see Chapter 123.

1. Decreased urine output, no evidence of renal failure based on laboratory findings or clinical examination. For mild dehydration only an increase in fluids (IV) or feedings may be necessary. For an infant only on breast-feeding who is dehydrated, supplement breast-feeding with formula.

2. Initial evaluation if renal failure suspected

   1. Bladder catheterization. This is done to see if urine is being made and to rule out lower urinary tract obstruction. It will not help in renal dysfunction or upper urinary tract obstruction. It may be helpful to keep an indwelling catheter in short term for strict intake and output (I&O).

   2. Evaluation of laboratory and ultrasound results. Based on the laboratory results and ultrasound, one should be able to identify whether the infant has prerenal, renal, or postrenal failure.

   3. Fluid challenge for diagnosis and initial management. A fluid challenge can be given in an infant without evidence of heart failure or volume overload (10–20 mL/kg of normal saline IV over 1–2 hours). If no response, this can be repeated once. An increase in urine output of ≥1 mL/kg/h indicates a prerenal cause. No response suggests intrinsic renal disease.

   4. Discontinue or restrict potassium from IV fluids. Restrict intake of phosphates.

   5. Evaluate the infant's medications. Adjust doses if necessary. Discontinue any nephrotoxic medications. If nephrotoxic medications cannot be discontinued, reduce the dose or use the minimal effective dose if possible.

   6. Strict I&O should be done. Weight the infant every 12 hours.

   7. For hypotension. Dopamine may increase renal perfusion.

3. Prerenal failure. The goal is to restore and maintain adequate renal perfusion. Because the kidneys are normal, prerenal failure is reversible once renal perfusion is restored.

   1. Treat the specific cause (eg, sepsis, NEC, and others).

   2. Provide volume resuscitation to restore renal perfusion. Depending how much fluid was given during the fluid challenge, another fluid challenge may be necessary to achieve euvolemia. Usual dose is 10–20 mL/kg over 1–2 hours of isotonic saline solution.

   3. Maintain adequate volume maintenance and replacement for any losses.

   4. Dopamine. Use of inotropic agents may be indicated in prerenal failure caused by hypoxia, acidosis, or indomethacin or in infants who develop hypotension. Renal dose of dopamine (1–3 mcg/kg/min) to improve renal perfusion is advocated by some, but no studies show that it improves survival. It increases urine output but does not prevent renal dysfunction or death. Cochrane review states that there is not enough evidence to give dopamine to prevent renal dysfunction specifically in indomethacin-treated preterm infants.

   5. Furosemide. May be indicated if there is oliguria and volume overload. Diuretics can help in fluid management but do not change the course of ARF/AKI. Furosemide (1–2 mg/kg/dose) can increase urine flow but limit doses due to ototoxicity, especially if there is no response noted.

4. Intrinsic renal disease. Supportive measures and treatment of the specific cause. Recovery and prognosis depends on the etiology.

   1. Pediatric nephrology consultation.

   2. Discontinue any nephrotoxic medications.

   3. Restrict fluid intake, and only replace insensible losses plus urine output. Consider potassium intake restriction.

   4. Follow serum sodium, potassium, calcium and phosphate, and acid-base balance. Infants with ARF can have hyponatremia (usually dilutional), hyperkalemia, hypocalcemia, hyperphosphatemia, and metabolic acidosis.

   5. Consider low-dose dopamine to increase renal blood flow (controversial). See Section V.C.4.

   6. Consider diuretics (furosemide, etc.) if fluid overload. Limit doses due to ototoxicity. See Section V.C.5.

   7. Follow blood pressure. Mild hypertension can occur.

5. Postrenal

   1. Urologic/pediatric surgical consultation.

   2. If obstruction is distal to the bladder. Perform initial bladder catheterization. Surgical vesicostomy may be indicated.

   3. If obstruction is proximal to the bladder. Urologic surgical intervention should be considered (eg, nephrostomy tubes or cutaneous ureterostomy).

   4. Neurogenic bladder. Initially managed with catheterization.

   5. Medications. Medications that cause urinary retention should be discontinued.

   6. Consider urinary tract infection prophylaxis with antibiotics.

6. Renal replacement therapy (RRT). Peritoneal dialysis (preferred method for neonates), hemodialysis, and hemofiltration with or without dialysis are considered only after medical management fails. RRT can be used in infants on ECMO with ARF/AKI and fluid overload. Indications include severe hyperkalemia, severe acidosis, severe hyponatremia, severe hypocalcemia, hyperphosphatemia, uremia, inadequate nutrition, and severe volume overload.

Andreoli  SP. Acute kidney injury in children. Pediatr Nephrol. 2009;4(2):253–263.
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Bridges  BC, Selewski  DT, Paden  ML  et al.. Acute kidney injury in neonates requiring ECMO. NeoReviews. 2012;13(7):e428.
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Chua  AN, Sarwal  MM. Acute renal failure management in the neonate. NeoReviews. 2005;6:e369–e376.
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Jetton  JG, Askenazi  DJ. Update on acute kidney injury in the neonate. Curr Opin Pediatr. 2012;24(2):191–196.
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Zappitelli  M, Selewski  DT, Askenazi  DJ. Nephrotoxic medication exposure and acute kidney injury in neonates. NeoReviews. 2012;13(7):e420.
CrossRef

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