Comparison of Ringer Lactate and Isotonic Acetate Solution as Maintenance Fluids in Children Undergoing Elective Laparoscopic Surgery

Fluid therapy is aimed to compensate for fasting which is required for surgery, to meet the ongoing fluid losses and to maintain electrolyte balance during surgery. Fluid deficit of a healthy child who is not fed parenterally may be estimated by multiplying hourly maintenance requirement for fluid by number of hours since the child's last oral intake (50% of deficit + maintenance in first hour, 25% of deficit + maintenance in second hour). Maintenance fluid therapy represents the volume of fluids and amount of electrolytes and glucose needed to replace anticipated physiological losses from breath, sweat and urine and to prevent hypoglycaemia. This maintains homeostasis while an individual is unable to control his/her own fluid intake while being operated. Replacement fluid represents the volume of fluid given to replace the volume lost during the surgical procedure. For 50 years, this therapy was based on Holliday and Segar's formula.

In 1957, Malcolm Holliday and William Segar published fluid management guide-lines for hospitalized children, which proposed to match children's water and electrolyte requirements on a weight-based calculation using: 100 ml/100 kcal for the first 10 kg of body weight, 50 ml/100 kcal for 11-20 kg and 20 ml/100 kcal for every kilogram of body weight above 20 kg. Their proposed maintenance electrolyte requirements of 3 meq/100 kcal of sodium (Na) per day and 2 meq/100 kcal of potassium (K) per day, were based upon the electrolyte composition of breast and cow's milk.

Once applied, these recommendations identified hypotonic fluid as the ideal maintenance fluid choice in hospitalized children, leading to the widespread use of 0.225% and 0.45% saline in this population. However, the widely used recommendations of Holliday and Segar did not consider the changing fluid and electrolyte requirements of a sick or postoperative child. Hypotonic fluid with a low sodium content (77 meq/l) and high percentage of electrolyte free water (78% EFW) can cause dilutional hyponatremia.Along with this, non-osmotic stimuli of anti-diuretic hormone (ADH) secretion in postoperative period makes the patient more vulnerable to hyponatremia. The primary stimulus for ADH release is an increase in osmolality however, many non-osmotic stimuli like nausea have also been identified as a potent non-osmotic stimulus for ADH release.Non osmotic causes of ADH release are broadly divided into hemodynamic and non-hemodynamic stimuli for its release. Hypovolemia, hypotension, hypoalbuminemia, congenital heart failure are some hemodynamic causes of non-osmotic secretion of ADH. Pneumonia, bronchitis, hypoxia, meningitis and brain tumour are some of the non-hemodynamic causes of ADH release.

Anti-diuretic hormone (ADH), is a neurophysial hormone which is synthesised in the supraoptic nuclei of the hypothalamus and released from the posterior pituitary gland. It binds to vasopressin V2 receptor in the basolateral membrane of the collecting duct, which leads to the insertion of aquaporin-2 receptors for retaining water in the body. By retaining water and decreasing urine output it increases the electrolyte free water in vascular compartment causing hyponatremia.Hyponatremia leads to hypotonicity of extracellular fluid (ECF) resulting in movement of water into intracellular space hence cell swells and cerebral edema occurs.Clinical presentation of acute hyponatremia (decrease in Na over ≤48 hours to <135meq/L) includes headache, lethargy and seizures, and potentially even respiratory and cardiac arrest secondary to brain stem herniation.2,3 These outcomes are more likely to be seen with severe acute hyponatremia (Na <130 mmol/L) and because of their higher brain/intracranial volume ratio, children are at increased risk for these sequelae compared with adults.Several studies have consistently showed that postoperative patients have an increased risk of developing hyponatremia.The incidence of hyponatremia after administration of hypotonic solutions varies from 11 to 31%.

Arieff et al, conducted a prospective clinical case study of 16 children and reviewed 24,412 children admitted for surgery. The main objective was to find out whether hyponatremia causes permanent brain damage or not. Over a period of 6 years, 16 children admitted in 5 tertiary hospitals and 9 community hospitals developed hyponatremia within 5 days of admission. At admission the sodium levels were 138 mmol/l. Patients became progressively lethargic, complained of nausea and vomiting after 2 hours of hypotonic fluid infusion. After 37 hours serum sodium was 115 mmol/l and urine osmolality was 676 mmol/kg. Among 16 patients, one was mentally retarded, 10 died and 5 were in permanent vegetative state. Four patients treated with IV sodium chloride (154 mmol/l and 512 mmol/l) showed an increase in sodium level from 108 to 138 mmol/l in 44 hours. Among 24,412 patients 83 patients developed postoperative hyponatremia out of which 7 died.