Total body water is distributed as follows: two-thirds in the intracellular space and one-third in the extracellular space. Seventy-five percent of the water in the extracellular space is located interstitially, while the remaining 25% is located intravascularly. For the extracellular fluid (ECF) space, sodium is the primary cation, while chloride and bicarbonate are the primary anions. For the intracellular fluid (ICF), potassium is the primary cation, while phosphate is the primary anion.
The tonicity (the measurement of osmotic pressure) of body fluids is tightly regulated within a physiologic range (osmolality of 275–290 mOsm/kg). While the body actually regulates tonicity, labwork measures osmolality (the concentration of solution, in terms of number of solute particles per kilogram). High osmolality (what is measured in a lab) does not always mean high tonicity. For example, urea, ethanol, methanol, and ethylene glycol freely cross cell membranes, so there is no water shift and no change in cell volume. In this case, tonicity is not affected, but osmolality is. Tonicity and osmolality align so closely in most situations, however, that these terms are used interchangeably in this chapter. Sodium concentration is the dominant factor in serum osmolality, as shown by the following estimation:
The two principal regulatory factors that maintain osmolality (and indirectly, the sodium concentration) in the normal range are antidiuretic hormone (ADH) and thirst.
ADH is the main determinant of free water excretion. It is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and stored in the posterior pituitary. Hypertonicity triggers its release, causing resorption of water by the kidney’s collecting tubules. ADH release is also triggered by hypovolemia (via volume receptors in the carotid sinuses), but not as powerfully. Other stimuli for ADH release include CNS disorders, meningitis, postoperative state, malignancies, pneumonia, pain, and stress (resulting in the syndrome of inappropriate antidiuretic hormone [SIADH]). When ADH is present, urine osmolality ranges from 300 to 1200 mOsm/kg, and urine specific gravity is >1.010. When ADH is absent, urine osmolality ranges from 50 to 80 mOsm/kg, and urine specific gravity is <1.005. The urine specific gravity is not as accurate a measure of ADH action as the urine osmolality, because specific gravity reflects the weight of particles in the urine, not just their number. For example, proteinuria may lead to a high urine specific gravity but a low urine osmolality.
A small rise in ECF tonicity stimulates thirst. Consequent decreased water excretion and increased water intake restore body fluid tonicity. High serum sodium and osmolality stimulate thirst and the intake of hypotonic fluids, while low serum sodium and osmolality suppress thirst. A low extracellular volume may increase thirst.
The renin/angiotensin system regulates ECF volume. Renin is produced by the juxtaglomerular cells of the kidney when they are hypoperfused. Renin stimulates angiotensin I production, which is then converted to angiotensin II by angiotensin-converting enzyme produced by the pulmonary and renal endothelium. Angiotensin II increases blood pressure by constricting the blood vessels, but also stimulates aldosterone secretion. Aldosterone is secreted by the adrenal cortex and acts on the distal tubules and collecting ducts to increase sodium and water resorption while also secreting potassium.
Thirst tells the body to add free water (lowering tonicity), ADH tells the kidneys to hold on to more free water (also lowering tonicity), and aldosterone tells the kidney to hold on to sodium, which pulls in water with it (increasing total volume without changing tonicity).
“Maintenance” fluids are the fluids a patient needs to receive in order to achieve homeostasis of fluid balance on an ongoing basis. The most common approach to calculation of maintenance water requirements is the Holliday-Segar Method.1 This method uses the water requirements for calorie expenditure in healthy children by calculating basal metabolic rates and total energy requirements during normal activity. By adding up normal insensible water losses from the skin and lungs as a result of metabolic activity, and losses in urine and the gastrointestinal tract, and then subtracting net gain from water oxidation, essentially 1 mL of water is needed for each kilocalorie of energy expended. Younger infants and children have higher metabolic rates and therefore require more fluids per unit of body weight than adolescents and adults. The Holliday-Segar method can be simplified and used to calculate fluids on a daily or hourly basis (Table 74-1). The hourly calculation is often referred to as the “4-2-1” rule.2-7 An important caveat to the Holliday-Segar Method is that it assumes the patient is healthy. Therefore it does not account for clinical conditions that alter insensible losses (respiratory distress, premature newborn, burns, other dermatologic impairment, etc.), urinary losses (SIADH, diuresis, etc.) or metabolic demand (fever, paralysis, neuroleptic malignant syndrome, etc.). In such cases, maintenance fluid rates require empiric adjustment.
The Holliday-Segar method refers only to water requirements and does not take into consideration electrolyte losses and needs. In healthy children, most electrolyte loss is through urine. An average of 3 mEq of Na+ and 2 mEq of K+ is lost for every 100 kcal of energy expended or 100 mL of maintenance fluid required per 24 hours. Estimations of 3 mEq/kg/day of Na+ per day and 2 mEq/kg/day of K+ are not as accurate. Alternatively, one can estimate electrolyte requirements by body surface area (BSA):
Using the BSA method, the electrolyte requirements are as follows:
The fluid deficit is the volume of fluids needed for a hypovolemic patient to become euvolemic.
The fluid deficit calculation is as follows:
If you don’t have a well weight, use Table 74-2 to estimate the patient’s degree of dehydration, as discussed in Chapter 73.
| A 7-year-old boy is admitted with a 2-day history of vomiting and diarrhea. He is estimated to be 7% dehydrated and vomited all attempts at oral rehydration in the emergency department. He was given a 20-mL/kg bolus of IV normal saline prior to transfer to the inpatient unit. His weight is 23 kg and his serum sodium level is 139 mEq/L. | ||||
| Water | Sodium | |||
| Calculation | Result | Calculation | Result | |
| Maintenance | ||||
| 1st 10 kg = 100 mL/kg | 10 kg × 100 mL/kg = 1000 mL | 1560 mL | 1560 mL × 3 mEq/100 mL | 47 mEq |
| 2nd 10 kg = 50 mL/kg | 10 kg × 50 mL/kg = 500 mL | |||
| >20 kg = 20 mL/kg | 3 kg × 20 mL/kg = 30 mL | |||
| Total Fluid Deficit | ||||
| = weight × % dehydration × 1000 mL/kg | 23 kg × 0.07 × 1000 mL/kg | 1610 mL | — | — |
| or | ||||
| = (normal wt – dehydrated wt) × 1000 mL/kg | ||||
| ECF Na+ Deficit | ||||
| = 0.6 × total fluid deficit × 140 mEq/L | — | — | 1.61 L × 0.6 × 140 mEq/L | 135 mEq |
| Correction for Sodium Derangement | ||||
| No sodium derangement | — | — | — | — |
| Total Requirements | — | 3170 mL | — | 182 mEq |
| Previous Replacement | 23 kg × 20 mL/kg | –460 mL | 0.46 L × 154 mEq/L | –71 mEq |
| Balance of Requirements | 3170 mL – 460 mL | 2710 mL | 182 mEq – 71 mEq | 111 mEq |
| Concentration of Saline Solution | 111 mEq ÷ 2.71 L | 41 mEq/L | ||
Sodium deficit calculation:
*In cases of acute dehydration, use 0.8. In cases of chronic dehydration, use 0.6. In acute dehydration (3 days or less), most of the fluid loss is from the extracellular space (80% extracellular, 20% intracellular). In chronic dehydration (longer than a 3-day period), there is greater intracellular fluid loss (60% extracellular, 40% intracellular). Intracellular fluid will move into the extracellular space, particularly the interstitial space, to make up for the loss of fluid in that space. Osmotic shifts will start to occur, making rapid fluid replacement more dangerous. In this case, fluid replacement should be slower and more controlled.
Combine the fluid deficit and electrolyte deficits to the maintenance requirements to determine the total amount of fluid and electrolytes that need to be replaced in 24 hours. Using that total volume and the total amounts of sodium and potassium needed, calculate the concentration of sodium and potassium for the patient’s intravenous fluids. Then, calclulate the hourly rate to administer that total volume over 24 hours. See Table 74-3 for an example that uses this approach to calculate a patient’s fluid needs. In addition, replace ongoing fluid losses 1:1 with the appropriate solution (Table 74-4).
| Water | Sodium | |||
|---|---|---|---|---|
| Calculation | Result | Calculation | Result | |
| Maintenance | ||||
| 1st 10 kg = 100 mL/kg | 9 kg × 100 mL/kg | 900 mL | 900 mL × 3 mEq/100 mL | 27 mEq |
| 2nd 10 kg = 50 mL/kg | ||||
| >20 kg = 20 mL/kg | ||||
| Total Fluid Deficit | ||||
| = weight × % dehydration × 1000 mL/kg | — | — | ||
| or | ||||
| = (normal wt – dehydrated wt) × 1000 mL/kg | (9 kg – 8 kg) × 1000 mL/kg | 1000 mL | ||
| ECF Na+ Deficit | ||||
| = 0.6 × total fluid deficit × 140 mEq/L | — | — | 1 L × 0.6 × 140 mEq/L | 84 mEq |
| Correction for Sodium Derangement | ||||
| Sodium deficit: | — | — | (134 – 122) × 9 kg × 0.6 | 65 mEq |
| = (desired Na+ – current Na+) × wt × 0.6 | ||||
| Total Requirements | — | 1900 mL | — | 176 mEq |
| Previous Replacement | 9 kg × 20 mL/kg | –180 mL | 0.18 L × 154 mEq/L | –28 mEq |
| Balance of Requirements | 1900 mL – 180 mL | 1720 mL | 183 mEq – 28 mEq | 148 mEq |
| Concentration of Saline Solution | 148 mEq ÷ 1.72 L | 86 mEq/L | ||
Oral rehydration is the best first therapy in uncomplicated mild and moderate dehydration (see Chapter 73).
Compared with IV therapy, there is increased risk of paralytic ileus and more treatment failures, but no difference in weight gain, duration of diarrhea, or total fluid intake at 6 hours, and a shorter length of stay.8 Parents generally prefer IV therapy over nasogastric hydration, however.9,10
Traditional recommendations regarding the time frame to fully correct moderate to severe hypovolemic dehydration from gastroenteritis have ranged from 24 to 48 hours.11,12 However, evidence from studies of oral or nasogastric rehydration therapy13 and from the emergency department setting14,15 demonstrates that a more rapid initial correction of hypovolemia using at least 20 mL/kg of isotonic crystalloid is safe and beneficial. Generally, this initial rapid correction involves boluses given over 5 to 10 minutes in urgent/emergent situations, and up to 20 to 30 minutes if less urgent. Controversy remains over rapid intravenous fluid resuscitation beyond 20 to 40 mL/kg.11,14,15 Holliday argues for more aggressive initial fluid resuscitation of the extracellular space, akin to volume repletion with severe burns (which calls for 4 mL/kg per percent of that is burned, the first half which administered over the first 8 hours). However, care must be taken to avoid dangerous complications from rapid fluids shifts in certain clinical conditions (such as hypernatremia, hyponatremia, diabetic ketoacidosis, severe illness with severe anemia, and cardiac or renal failure).16 Development of crackles or hepatomegaly may indicate that the patient’s cardiorespiratory status is not tolerating rapid fluid therapy.
Use of the traditional Holliday-Segar method typically results in choosing hypotonic fluids (0.2 normal saline [NS] or 0.5 NS). Over the past 10 years, however, there has been considerable focus in the medical literature about an alternative approach to IV fluid selection, shifting away from physiologic calculations and toward outcomes. In particular, this newer approach eschews hypotonic IV fluids in order to minimize the chance of cerebral edema and brain herniation, rare but devastating iatrogenic complications of unrecognized severe hyponatremia.17
There is now solid evidence that the use of hypotonic fluids for maintenance in the pediatric settings causes sodium concentration to drop significantly lower than isotonic fluid use does.18-24 The evidence is particularly strong in the postsurgical and intensive care population, who carry higher risk for SIADH. Some authors have cautioned against use of isotonic fluids as a strategy to mitigate harm from SIADH, considering that the treatment for SIADH is fluid restriction, not changing the sodium concentration of the fluids.25,26 Studies examining routine reduction of maintenance rates have failed to document reduced rates of hyponatremia, however.20,21 Critics of routine isotonic saline at maintenance rates also raise concern that this approach provides excessive sodium chloride, setting up edema and potentially exacerbating acidosis by causing hyperchloremic acidosis.27
To date, the most important potential benefit of isotonic saline at maintenance rates—reduced rates of cerebral edema and herniation—has not been demonstrated. Given the rarity of this outcome, however, only extremely large, likely retrospective database studies would have the power to answer this question.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
