The Effects of
Chloride and Acetate on Metabolic Acidosis in
Parenterally Fed Preterm Neonates:
A Prospective Randomised Double Blind Controlled Trial.

F Peters, S Ryan, LA Matthew, K Chan*,
Liverpool Women's Hospital NHS Trust and *Liverpool John Moores University.
Received: October 1997

journal

 

Introduction

 Preterm neonates have, an obligate sodium loss frequently resulting in hypernatraemia. In current practice,, the a administration of additional sodium chloride in the parenteral nutrition (PN) solution frequently results in hyperchloraemia(1). The effect of hyperchloraemia on acid-base balance has been reported and suggestions of partially substituting the chloride content of PN solutions with acetate have appeared to improve acid-base balance(1,2).

Hyperchloraemia and metabolic acidosis frequently co-exist in the preterm. A pilot study undertaken on the Regional Neonatal Intensive Care Unit showed a direct causal relationship between base deficit and plasma chloride concentration. The aim of the study was to further investigate the reduction of the incidence of hyperchloraemia, metabolic acidosis, the duration of ventilation by replacing PN chloride with acetate and the relationship between hyperchloraemia and metabolic acidosis.

Method

Sixty consecutively born preterm neonates less than 32 week. gestation were randomised into the study for the first ten days of life. Standard dextrose-electrolyte solutions were administered for the first two days, with PN initiated from the third day onwards. Electrolytes were monitored daily and adjusted as required. Thirty neonates received the current PN regime with the prescribed amount of sodium as the chloride salt, and thirty received a similar regime with part of the prescribed requirement of sodium as the chloride salt (maximum of 3 mmol/kg/day) and the balance as the acetate.

Chloride intake, plasma chloride, parameters of metabolic acidosis (blood gases pH, bicarbonate, base excess, carbon dioxide partial pressure pCO2), inotrope, albumin and bicarbonate infusions (for acidosis treatment), ventilators requirements and duration were monitored daily.

Results

Both groups were similar for gestational age, birth weight (Table 1) and total chloride intake prior to commencing PN. From day 3 onwards, mean chloride intake and plasma chloride remained within the recommended range in the Chloride-Acetate PN group (7 out of 28 developed hyperchloraemia) but rose significantly in the Chloride PN group (23 out of 30 developed hyperchloraemia) (p<0.001) (Table 1).

Blood gas base excess, (p<0.001), bicarbonate, (p<0.001) and pH (p<0.005) levels, were higher in the acetate group with majority of the levels within the normal range compared to those in the Chloride PN group (Table 1). No significant difference, in pCO2 was observed between the groups until days 6 to 8 (p<0.05), when levels were higher in the Chloride-Acetate PN group.

A reduced number of albumin (p<0.00 1) and sodium-bicarbonate (p<0.00 1) infusions were administered in the acetate group (Table 1). There was no difference in inotrope infusion between the groups.

Mean ventilatory rates and pressures fell progressively in both groups but at a slightly faster rate in the acetate group. This was not statistically significant. The median duration of ventilation was longer in the Chloride PN group (12 days.) than the Chloride-Acetate PN group (4.5 days) but this was not statistically significant because of the large variability observed.

A direct relationship was observed between plasma chloride and the parameters of metabolic acidosis.

Conclusion

Hyperchloraemia potentiates the incidence of metabolic acidosis. The partial substitution of chloride ions with acetate (4mmol/ kg/ day maximum) in the PN solution significantly reduces the incidence of hyperchloraemia, metabolic acidosis and its treatment. The duration of ventilation is also reduced to a lesser degree.

Table 1. Characteristics of The Study Group

PARAMETERS
±SEM (range) 		CHLORIDE
GROUP 		ACETATE
GROUP
Mean gestation.
(weeks) 		27
(24-31) 		27.7
(24-31)
Mean birth weight
(Kg) 		1.06 -10.1
(0.66-1.69) 		1.01 ±0.1
(0.66-1.67)
Total number ventilated 29 27
Mean chloride intake
(mmol/kg/day) 		6.23 ±3.2
(2.03-23.05) 		3.63 ±1.9
(0.36~12.46)
Mean acetate dose
(mmol/kg/day) 		  3.13 ±0.51
(0- 14.16)
Mean daily plasma chloride
(mmol/1) 		111.1 ±2.7
(94-123) 		106.6 ±1.7
(82-122)
Mean daily plasma base excess
(mmol/l)		 5.0 ±0.6
(-26 - 4.6)		 -1.28 ±1.0
(-23 - 22.2)
Mean daily plasma bicarbonate
(mmol/l)		 20.47 ±0.6
(6-29) 		24.30 ±1.0
(12-53)
Mean daily plasma pH 7.3 1
(6.9 - 7.5 9) 		7.33
(6.67 - 7.57)
Mean volume albumin infusions
(ml/kg/day)		 11.58 ±2.9
(0-77.27) 		6.24 ±1.7
(0-92.31)

results

References

Groh-Wargo RD. Ciaccia A. Moore J.
Neonatal metabolic acidosis: Effects of chloride from normal saline flushes. JPEN 1988; 12(2):159-161

Richards CE. Drayton M. Jenkins H. Peters, TJ.
Effect of different chloride infusion rates on plasma base excess during neonatal PN. Acta Paediatric Int. J. Paediatr. 1993;82(8):678-682

Cheng K. Ryan SW.
Relationship between chloride status and metabolic acidosis in preterm neonates requiring PN. Proceedings. 67th annual meeting, British Paediatric Association. 1995;67:59 (abstract)

 


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