The plasma osmolality is tightly controlled between 285 and 295 mOsm/kg through regulation of water intake and urinary water losses. A small increase in the plasma osmolality stimulates thirst. Urinary water losses are regulated by the secretion of antidiuretic hormone (ADH), which increases in response to an increasing plasma osmolality. ADH, by stimulating renal tubular reabsorption of water, decreases urinary water losses. Control of osmolality is subordinate to maintenance of an adequate intravascular volume. When significant volume depletion is present, ADH secretion and thirst are stimulated, regardless of the plasma osmolality.
Volume depletion and volume overload may cause significant morbidity and mortality. Because sodium is the principal extracellular cation and is restricted to the ECF, adequate body sodium is necessary for maintenance of intravascular volume. The kidney determines sodium balance because there is little homeostatic control of sodium intake, although salt craving occasionally occurs, typically in children with chronic renal salt loss. The kidney regulates sodium balance by altering the percentage of filtered sodium that is reabsorbed along the nephron. The renin-angiotensin system is an important regulator of renal sodium reabsorption and excretion. The juxtaglomerular apparatus produces renin in response to decreased effective intravascular volume. Renin cleaves angiotensinogen, producing angiotensin I, which angiotensin-converting enzyme converts into angiotensin II. The actions of angiotensin
Figure 32-1 Compartments of total body water, expressed as percentage of body weight, in an older child or adult. (From Greenbaum LA: Pathophysiology of body fluids and fluid therapy. In Kliegman RM, Stanton, BF, St Geme JW, et al, editors: Nelson Textbook of Pediatrics, 19th ed. Philadelphia, 2011, Saunders, p 212.e1.)
II include direct stimulation of the proximal tubule to increase sodium reabsorption and stimulation of the adrenal gland to increase aldosterone secretion, which increases sodium reabsorption in the distal nephron. In contrast, volume expansion stimulates the synthesis of atrial natriuretic peptide, which increases urinary sodium excretion.
Maintenance intravenous (IV) fluids are used in children whocannot be fed enterally. Along with maintenance fluids, childrenmay require concurrent replacement fluids if they have excessive ongoing losses, such as may occur with drainage from a nasogastric tube. In addition, if dehydration is present, the patient alsoneeds to receive deficit replacement (see Chapter 33).
Maintenance fluids are composed of a solution of water, glucose, sodium, potassium, and chloride. This solution replaces electrolyte losses from the urine and stool, as well as water losses from the urine, stool, skin, and lungs. The glucose in maintenance fluids provides approximately 20% of the normal caloric needs of the patient. This percentage is enough to prevent the development of starvation ketoacidosis and diminishes the protein degradation that would occur if the patient received no calories.
Maintenance fluids do not provide adequate calories, protein, fat, minerals, or vitamins. Patients should not remain on *The maximum total fluid per day is normally 2400 mL.
†The maximum fluid rate is normally 100 mL/hr.
maintenance therapy indefinitely; parenteral nutrition (see Chapter 34) should be used for children who cannot be fed enterally for more than a few days.
Daily water losses are measurable (urine and stool) and not measurable (insensible losses from the skin and lungs). Failure to replace these losses leads to a thirsty child and, ultimately, a dehydrated child. Table 32-1 provides a system for calculating 24-hour maintenance water needs based on the patient’s weight. Sodium and potassium are given in maintenance fluids to replace losses from urine and stool.