MANAGEMENT — The treatment of ARF that does not respond to fluid challenge, as described above, depends upon the underlying etiology, severity, and complications. The general approach consists of Maintenance of fluid and electrolyte balance Avoidance of life-threatening complications Adequate nutritional support Treatment of the underlying cause
Fluids — Fluid administration should be limited to estimated insensible water losses plus the urine output. Infants with renal failure should be weighed every 12 hours and fluid administration adjusted accordingly.
Daily insensible loss in newborns increases with decreasing birth weight, as follows [34,42,43]: >2500 g — 15 to 25 mL/kg 1500 to 2500 g — 15 to 35 mL/kg <1500 g — 30 to 60 mL/kg
Infants cared for under radiant warmers rather than incubators may need 25 to 100 percent more fluid. In addition, the daily fluid increment typically required by infants receiving phototherapy is approximately 20 mL/kg.
Hyperkalemia — Depending upon the severity and the rate of onset, hyperkalemia can be mild and asymptomatic or so severe as to constitute a medical emergency. Electrocardiographic findings associated with hyperkalemia consist of peaked T waves, which typically is the earliest change, followed by flattened P waves, increased PR interval, and widening of the QRS complex. Bradycardia, supraventricular or ventricular tachycardia, and ventricular fibrillation may occur. Muscle weakness is another potential manifestation that can be difficult to distinguish from that seen with severe illness alone.
A plasma potassium concentration above 6 to 7 meq/L is potentially life-threatening. Immediate therapy is warranted if electrocardiographic changes are present, regardless of the degree of hyperkalemia.
The following modalities are listed according to their rapidity of action; all may be beneficial :
-Reversal of the effect of hyperkalemia on the cell membrane by infusion of 10 percent calcium gluconate (0.5 to 1.0 mL/kg IV over five minutes). Calcium is generally given only for severe, life-threatening hyperkalemia.
-Promotion of potassium movement from the extracellular fluid (ECF) into the cells. This can be achieved by the administration of sodium bicarbonate (1 to 2 meq/kg IV over 5 to 10 minutes), particularly if the infant is acidemic, and the administration of insulin as a bolus (0.05 units/kg human regular insulin with 2 mL/kg of 10 percent dextrose in water), followed by a continuous infusion of insulin (0.1 units/kg per hour with 2 to 4 mL/kg per hour of 10 percent dextrose in water). If these modalities are ineffective, stimulation of cellular potassium uptake can also be achieved with beta adrenergic receptor agonists, such as albuterol (4 to 5 mcg/kg IV over 20 minutes or 2.5 mg by nebulization) or salbutamol (4 mcg/kg IV).
The above interventions only transiently lower the plasma potassium concentration. Additional therapy is required to remove potassium from the body. The first step is to increase the urine output with furosemide (1 mg/kg per dose) in infants with adequate urine output.
In severely oliguric or anuric patients, Kayexalate, an ion exchange resin, can be administered in a dose of 1 g/kg dissolved in saline for rectal administration or in 10 percent dextrose in water for enteral administration. Exchange resins should be avoided, if possible, in small preterm infants who may develop gastric bezoars or cecal perforation. Other complications include bowel opacification, hypernatremia, fluid retention, and constipation [34,44].
Renal replacement therapy should be considered if these measures fail to improve hyperkalemia.
Metabolic acidosis — In addition to the treatment of hyperkalemia, metabolic acidosis should be corrected if the plasma bicarbonate concentration falls below 16 meq/L or the arterial pH is less than 7.20 to 7.25. Bicarbonate therapy is not warranted if the acidosis is primarily respiratory.
Correction of metabolic acidosis is accomplished by administering sodium bicarbonate in a dose that can be estimated from the following formula:
Bicarbonate dose= (16 — serum bicarbonate concentration) x 0.4 x body weight (kg)
An alternative approach is to give bicarbonate empirically in a dose of 1 to 2 meq/kg.
Depending upon the severity of metabolic acidosis, the bicarbonate dose can be given intravenously over five to 10 minutes or added to the intravenous fluids and given over several hours. Rapid correction by bolus infusion should be avoided because of the risk of hypertension, fluid overload, and intracranial hemorrhage.
Hypocalcemia and hyperphosphatemia — Hypocalcemia generally is not treated with intravenous calcium gluconate unless the patient is symptomatic or the hypocalcemia is severe.
Among patients who are hyperphosphatemic, lowering the serum phosphate concentration will also tend to raise the serum calcium. Phosphorus intake should be restricted which, in infants taking enteral feedings, can be accomplished by using a formula low in phosphorus. Oral phosphate binders such as calcium carbonate can be used to decrease intestinal absorption.
Hyponatremia — Hyponatremia in newborns is almost always due to dilution that results from the intake of water that cannot be excreted. Therapy generally consists of restricting free water intake, which usually results in a gradual return of the serum sodium to normal levels. However, if neurologic signs such as seizures or lethargy develop or if the serum sodium concentration is extremely low (<120 meq/L), urgent partial correction is needed with hypertonic saline. Additional correction of hyponatremia should be based upon calculations of the sodium deficit, which is equal to the product of the volume of distribution of the serum sodium concentration (the total body water) times the sodium deficit per liter (ie, 140 minus the serum sodium concentration)
Nutrition — Nutritional support is essential for infants with ARF and should consist of a minimum of 50 kcal/kg per day. Infants who are able to take enteral feedings should be given a formula that has a low renal solute load and low phosphate content. However, the need for fluid restriction makes it difficult to meet the caloric needs of an oliguric infant. As a result, daily loss of 0.2 to 1 percent of body weight usually persists beyond the first week of age [44]. The weight loss is not reversed until the clinical condition improves and nutrition is adequate.
Most affected infants are critically ill and require parenteral nutrition. Such infants should receive amino acids up to a maximum of 1.5 g/kg per day and intravenous lipid solution up to a maximum of 2 g/kg per day. The concentration of glucose and solutes such as sodium, potassium, calcium, and phosphorus depend upon the infant's weight, serum electrolyte concentrations, the severity of the renal failure, and whether or not the patient is on dialysis.
Hypertension — Approximately 10 to 20 percent of infants with ARF have hypertension. This is usually due to fluid overload. Treatment is similar to infants without ARF.
Renal replacement therapy — Renal replacement therapy should be considered if appropriate fluid and electrolyte balance and adequate nutrition cannot be maintained because of persistent oliguria or anuria. We consider renal replacement therapy in infants who, despite appropriate therapy, have severe acidosis (serum bicarbonate concentration <12 meq/L), hyperkalemia (plasma potassium concentration 8 meq/L), hyponatremia (serum sodium concentration 120 meq/L), or volume overload with heart failure, pulmonary edema. Dialysis is performed rarely in severe hypertension that is not responsive to medications and is associated with central nervous system signs such as seizures or with heart failure.
The question of whether to institute renal replacement therapy in a newborn with no expectation of recovery of renal function or with severe multisystem failure is difficult. Decisions should be made after considerable discussion with the neonatologist, nephrologist, other consultants as needed, and the family.
Available renal replacement modalities for the management of ARF in newborns include hemodialysis, peritoneal dialysis, and hemofiltration (with or without dialysis). The choice of modality is influenced by the clinical presentation, the presence or absence of multisystem failure, and the indication for renal replacement therapy [45].
Hemodialysis and peritoneal dialysis each provide specific benefits [46]: Hemodialysis offers a more rapid change in plasma solute composition and more rapid removal of excessive body water. However, this may not be tolerated by hemodynamically unstable patients and is technically challenging in newborns. Peritoneal dialysis is less efficient in altering blood solute composition and in fluid removal. However, it can be applied continuously and is therefore well tolerated by hemodynamically unstable patients. Unlike hemodialysis and hemofiltration, systemic heparinization is not required.
Peritoneal dialysis is preferred in newborns, even in those of low birth weight [47,48]. It is safe and effective and technically simpler and less expensive than hemodialysis and hemofiltration, requiring only minimal equipment. It can be initiated immediately after the dialysis catheter is placed and can be done as soon as three days after major abdominal surgery [49].
Morbidity and mortality are high in newborns undergoing peritoneal dialysis and are related to the infant's underlying diagnosis and clinical condition. In one series, 31 infants with renal failure (n = 20) or metabolic disorders (n = 11) underwent dialysis at less than 60 days of age, and 19 (61 percent) died [50]. Complications included peritonitis, obstruction of the dialysis catheter, leaking dialysate, and inguinal or umbilical hernias. Five of the 12 survivors remained on chronic dialysis awaiting renal transplantation.
The use of continuous venovenous hemodiafiltration (CVVHD) is increasing in newborns. Compared with peritoneal dialysis and hemodialysis, CVVHD allows more precise fluid and metabolic control, decreases hemodynamic instability, and, in patients with sepsis or multiorgan system failure, enhances the removal of cytokines [51,52].
PROGNOSIS — The prognosis of ARF in newborns depends upon the underlying condition and its severity and reversibility. Mortality is high and a substantial number of patients develop chronic renal failure. In a review of ARF in neonates, mortality was as high as 60 percent in patients with oliguric ARF and up to 86 percent in those with congenital heart disease or urinary tract anomalies [4]. Among the survivors of oliguric ARF caused by asphyxia, vascular thrombosis, hypotension, and toxins, 40 percent had persistently low creatinine clearance. In comparison, the prognosis was excellent in newborns with nonoliguric renal failure.
Other small series have evaluated subsets of newborns with ARF [1,16,53]. The following illustrate the range of findings: Among 14 newborns with ARF due predominantly to hypoxemia and hypotension, five died during the acute phase [16]. Five of the nine survivors had residual renal damage. In a series of 16 newborns, ARF was due to perinatal asphyxia in nine, renal anomalies in four, and congenital heart disease in three [1]. Four infants died, all with oliguric renal failure; all were anuric four or more days and had no uptake on radionuclide scintigraphy. The serum creatinine concentration in the survivors was normal.
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الإثنين سبتمبر 29, 2008 6:04 am
