Acute peritoneal dialysis in infants weighing <1500 g

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Clinical and laboratory observations

The Journal of Pediatrics January 1987

T a b l e II. Activities of glycine cleavage system and individual enzyme components in placenta of fetus at risk for nonketotic hyperglycinemia, control fetuses at week 12 of gestation, and full-term ~ormal babies

Activity (/~mol product/g protein/hr) Source of placenta

Glycine cleavage

P-protein

H-protein

T-protein

Llpoarnide dehydrogenase

Fetus at risk for NKH Control fetus (12 wk) Control fetus (12 wk) Control fetus (12 wk) Control infant (38 wk) Control infant (39 wk)

0.2 4.8 2.5 4.1 0.8 0.8

4.4 6.6 4.5 . . .

6.7 10.4 5.1

0 2.8 2.6

865.5 1582.4 734.5

5. Motokawa T, Kikuchi G. Glycine metabolism by rat liver mitochondria: reconstitution of the reversible glycine cleavage system with partially purified protein components. Arch Biochem Biophys 1974;164:624. 6. Gitzelmann R, Steimann B. Clinical and therapeutic aspects of non-ketotic hyperglycinemia. J Inher Metab Dis 1982; 5:113. 7. Matalon R, Naidu S, Hughes JR, Michals K. Nonketotie hyperglycinemia: treatment with diazepam, a competitor for glycine receptors. Pediatrics 1983;71:581. 8. Garcia-Castro J, Isales-Forsyth I, Levy H, et al. Prenatal diagnosis of nonketotic hyperglycinemia. N Engl J Med 1982;306:79.

. . .

. . .

. . .

9. Wendt LV, Simil/i S, Ruokonen A, Hartikainen-Sorri AL. Problems of prenatal diagnosis of nonketotie hyperglycinemia. J Inher Metab Dis 1983;6:112. 10. Mesvage C, Nanee CS, Flannery DB, Weiner DL, Suehy SF, Wolf B. Glycine/serine ratios in amniotic fluid: an unreliable indicator for the prenatal diagnosis of nonketotic hyperglycinemia. Clin Genet 1983;23:354. 11. Bachmann C, Mihatsch M J, Baumgartner R, et al. Nichtketotische hyperglyziniimie: perakuter Verlauf im Neugeborenenalter. Helv Paediatr Aeta 1971;26:228. 12. Reid DW, Gampbell D J, Yakymuyshyn LY. Quantitative amino acids in amniotic fluid and maternal plasma in early and late pregnancy. Am J Obstet Gynecol 1971;111:251.

Acute peritoneal dialysis in infants weighing <1500 g B. T. Steele, M.D., A. Vigneux, R.N., S. Blatz, R.N., M.Ed., M. Flavin, M.D., a n d B. Paes, M.D. From the Departments of Pediatrics and Nursing, McMaster University, Hamilton, Ontario, Canada

Acute renal failure is not uncommon in neonatal intensive care units. Some infants have a transient, mild impairment of renal function, whereas others have progressive anuric renal failure, sometimes accompanied by multiple organ failure. Apart from occasional case reports, 1-3there is little published information on dialysis techniques or results in very low birth weight neonates. W e describe the results of a simple dialysis procedure used in 13 infants weighing <1500 g.

Submitted for publication May 28, 1986; accepted Aug. 18, 1986. Reprint requests: B. T. Steele, M.D., Department of Pediatrics, McMaster University Medical Centre, 1200 Main St., W., Hamilton, Ontario, Canada L8N 3Z5.

METHODS Between July 1983 and July 1985, 13 infants weighing between 380 and 1400 g (mean 894 g) required acute peritoneal dialysis. In 12 infants dialysis was required for acute, anuric renal failure (Table). Severe hyaline membrane disease with persistent pulmonary hypertension, associated with hypotensive episodes, was the most common explanation for acute renal failure. Five infants had hyperkalemia associated with arrhythmias, and 10 had severe fluid retention with generalized edema. The degree of fluid retention had, in all cases, increased ventilation requirements and severely limited fluid intake. As a result, all had required at least one dose of 20% dextrose to correct hypoglycemia. One infant did not have renal failure but required dialysis to correct arrhythmias second-

Volume 110 Number 1

ary to hyperkalemia (K § 15.2 mmol/L) after accidental intravenous administration of potassium chloride. Dialysis technique. The skin of the abdomen was cleaned with povidone-iodine solution, followed by sterile water. A No. 14 Angiocath (Deseret Medical, Inc., Sandy, Utah) was inserted through the lateral abdominal wall, in an effort to position the tip of the catheter deep in the contralateral iliac fossa or pelvis. The length of the catheter was used to estimate the point of entry, and the catheter and dialysis tubing were held in place with a clean plastic dressing. Pediatric intravenous lines were used to deliver the dialysis fluid, which was passed through a fluid warmer. Y and T connectors were used to minimize the weight of tubing lying on the abdomen. Drainage of fluid was completed with intravenous extension tubing and a Sims adapter (Pharmaseal, American Hospital Supply, Mcgaw Park, Ill.) to a urine meter. RESULTS The 13 infants each required peritoneal dialysis for 12 to 210 hours (mean 51 hours). All received 1.5% Dianeal solution (Travenol Labs, Inc. Deerfield, IlL) with 500 U heparin added to each liter. The volume of each exchange varied between 10 and 50 ml, with the intention of using approximately 20 ml/kg. In 10 infants ultrafiltration was excellent. (4.83 ___ 3.36 m L / k g / h r , mean +_ SD). Ultrafiltration was not achieved in patients 3 and 4, both of whom had poor peripheral perfusion, and in patient 1, who did not have renal failure. The serum potassium concentration became normal in all but patient 4. Poor drainage, with leakage of diatysate from the catheter exit site, initially occurred in three patients, two of whom required a second peritoneal catheter. In these three infants hyperglycemia also developed, requiring insulin for 12 hours in one infant. Bleeding during the insertion of the peritoneal catheter was not seen in any patient, even though eight patients had evidence of disseminated intravascular coagulation. Antibiotics were not given routinely with the peritoneal catheter insertion, and there were no episodes of peritonitis. Ten patients, however, had been given antibiotics for presumed sepsis prior to dialysis, and they were given intraperitoneal ampicillin and amikacin without any further intravenous doses. A systematic study of glucose absorption was not done in all patients, but studies in four patients showed absorption between 200 and 300 mg glucose/kg/hr. Six infants died, including five who remained anuric. Full supportive therapy was withdrawn in four of these infants because of severe and irreversible brain damage. Patient 7 had the clinical features of hepatorenal syndrome, and died of combined hepatic and renal failure. Patient 8 died of an unexplained cardiac arrhythmia, after

Clinical and laboratory observations

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renal failure had improved; this infant had mild acute tubular necrosis. In the other three infants autopsies demonstrated severe renal Cortical and medullary necrosis. Seven infants survived, but three of these subsequently died of bronchopulmonary dysplasia in the next 4 to 8 weeks. All four long-term survivors have normal urinary fndings and normal serum creatinine concentration (follow-up 6 to 26 months). DISCUSSION Because there are few studies of acute renal failure in very low birth weight infants, its incidence is unknown. In one study, 7% of all deaths in a neonatal intensive care unit were attributed to renal failure. 4 Hemodialysis and continuous arteriovenous hemofiltration are both technically difficult because they require access to and maintenance of a good arterial blood flow. Continuous arteriovenous hemofiltration has recently been described in a 1300 g infant, s but satisfactory ultrafiltration can be achieved with peritoneal dialysis. Our experience suggests that a simple peritoneal dialysis procedure is technically possible in very small infants, and in many cases may alter both early morbidity and mortality. The insertion of peritoneal dialysis catheters can be associated with severe abdominal wall bleeding or perforation of the intestine, aorta, or inferior vena cava. 6 Commercially available dialysis catheters are unnecessarily large for these low birth weight infants and are thus more likely to produce damage. We initially used a No. 14 angiographic catheter with several side holes (made with a 22-gauge needle) to enhance drainage. This occasionally produced problems, however, with small pieces of mesentery lodging in the side holes and consequently blocking the lumen of the catheter. We no longer make side holes in the catheter, and such problems have not occurred. Patency of the catheter may be helped by the addition of heparin, and in the concentration used we did not see bleeding. Leakage of dialysate around the catheter at the exit site can be troublesome, but recent success with a drop of collodion at the exit site has been encouraging. A decrease in the mortality and morbidity from acute renal failure in older infants and children has been attributed to the earlier use of dialysis.7 This may also apply to the very low birth weight infant. At least two patients in our series received treatment at a late stage, when severe fluid overload adversely affected oxygenation and tissue perfusion. Dialysis was not effective in either patient, presumably because of poor circulation to the peritoneal membrane. Hyperkalemia can be treated with oral or rectal ion exchange resins, but this is technically

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Clinical and laboratory observations

The Journal of Pediatrics January 1987

Table. Clinical data

Patient 1 2 3 4 5 6 7 8 9 10 11 12 13

Cause of renal failure -Hepatorenal syndrome Severe oligohydramnios; anuria from birth RDS, PPH RDS, PPH RDS, PPH Post-PDA ligation following indomethacin RDS, PPH Severe oligohydramnios, anuria from birth RDS, PPH Post-PDA ligation following indomethacin RDS, PPH Severe oligohydramnios, anuria from birth

Weight at dialysis (g)

Age at dialysis (day)

Time on dialysis (hr)

Hyperkalemia Fluid overload Fluid overload

1400 1320 1270

2 23 4

36 210 70

Hyperkalemia, fluid overload Fluid overload Hyperkalemia Fluid overload, hyperkalemia

1000 1000 900 850

5 4 17 19

12 12 24 103

Fluid overload Fluid overload

800 800

3 3

66 22

Hyperkalemia Fluid overload

770 680

6 15

6 67

Fluid overload Fluid overload

450 380

3 2

14 72

Indication for dialysis

PDA, Patent ductus arteriosus; PPH, persistent pulmonary hypertension; RDS, respiratory distress syndrome. difficult in small infants, and in our experience, rarely effective. Since becoming more familiar with this technique as a safe and simple procedure, we now use peritoneal dialysis at a n earlier stage of acute renal failure. A m a j o r difficulty with acute renal failure in small neonates is t h a t intravenous fluid requirements become severely limited, yet a steady state of glycemic homeostasis m u s t be achieved. Dialysis with a glucose-containing fluid will m a i n t a i n a n a d e q u a t e blood glucose concentration and

allow sufficient fluid removal to provide early total parenteral nutrition. Thus the caloric requirements of the sick p r e m a t u r e neonate can be maintained; this improved nutrition m a y also be i m p o r t a n t for renal and other organ recovery? In the patients who were not treated late, a large amoun~ of fluid loss was possible; indeed, ultrafiltration was often so good t h a t careful monitoring was required to avoid subsequent circulating volume depletion. In the two patients in whom ultrafiltration was not

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Clinical and laboratory observations

Volume of exchange (ml)

Ultrafiltration (ml/kg/hr)

50 20 30

0 3.8 0

Survived Died Died

20 20 20 20

0 10 3.8 5.9

Died Sur,/ived Died (nonrenal) Died

15 15

4.4 6.2

Died (nonrenal) Survived

20 20

9.7 4.9

Died (nonrenal) Survived

10 10

7.0 7.1

Died Died

Outcome

possible, a solution with higher osmolalities, that is, 2.5% and 4.25% Dianeal (osmolalities 397 and 485 m O s m / L , respectively) did not make any difference. The change merely worsened the hyperglycemia; thus 1.5% Dianeal solution would appear to be adequate for dialysis in these infants if tissue perfusion is adequate. During dialysis the blood sugar concentration rises rapidly because of absorption of dialysate glucose. The degree of hyperglycemia was minimized by reducing the concentration of dextrose in all

12 9

intravenous solutions. Some sick neonates are not able to Convert dialysate lactate to bicarbonate, and a dialysate solution containing bicarbonat e can be prepared and used2 We did not find this necessary in any of the 13 infants, none of whom had persisting metabolic acidosis. This simple dialysis procedure can be used safely to correct fluid overload or hyperka|emia. With increasing experience from a team approach, we believe that early dialysis i s likely to reduce both the morbidity and mortality of acute renal failure in small neonates.

REFERENCES 1. Kanarek KS, Root E, Sidebottom RA, William PR. Successful peritoneal dialysis in an infant weighing less than 800 grams. Clin Pediatr 1982;21:167. 2. Berger A, Garty J, Tirosh E. Peritoneal dialysis in a premature infant with hyponatremia, hypervolemia and anuria, isr J Med Sci 1983;19:51. 3. Nash MA, Russo JC. Neonatal lactate acidosis and renal failure: the role of peritoneal dialysis. J PEDIATR 1977; 91:101. 4. Jones AS, James E, Bland H, Groshong T. Renal failure in the newborn. Clin Pediatr 1979;18:286. 5. Lieberman KV, Nardi L, Bosch JP. Treatment of acute renal failure in an infant using continuous arteriovenous hemofiltration. J PEDIATR 1985;107:646. 6. Vaamonde CA, Michael VP, Metzger RA, Carroll KE. Complications of acute peritoneal dialysis. J Chronic Dis i975;28:637. 7. Lieberman E. Management of acute renal faiilure in infants and children. Nephron 1973;11:193. 8. Abel RM, Beck CH, Abbot WM, Ryan J, Barnett GO, Fischer JE. Improved survival from acute renal failure after treatment with intravenous essential L-amino aids an d glucose. N Engl J Med 1973;288:695.