Fluid and electrolyte therapy

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Chapter 85 Fluid and electrolyte therapy

The management of patients’ fluid and electrolyte status requires an understanding of body fluid compartments as well as an understanding of water and electrolyte metabolism. These principles will be considered along with the commonly encountered fluid and electrolyte disturbances. Recent evidence for the use of fluid therapy in a number of common clinical scenarios will also be presented.

FLUID COMPARTMENTS (Table 85.1, Figure 85.1)

TOTAL BODY WATER

In humans, water contributes approximately 60% of body weight, with organs varying in water content (Table 85.2). The variation of the percentage of total body weight as water, between individuals, is largely governed by the amount of adipose tissue. The average water content as a percentage of total body weight is 60% for males and 50% for females. Total body water as a percentage of total body weight decreases with age, due to a progressive loss of muscle mass, causing bone and connective tissue to assume a greater percentage of total body weight¹^–³ (Table 85.3).

Table 85.1 Body fluid compartments

Fluid compartment	Volume (ml/kg)	% Total body weight
Plasma volume	45	4.5
Blood volume	75	7.5
Interstitial volume	200	20
Extracellular fluid volume	250	25
Intracellular fluid volume	350	35
Total body fluid volume	600	60

Figure 85.1 Body fluid compartments.

Table 85.2 Water content of various tissues

Tissue	% Water content
Brain	84
Kidney	83
Skeletal muscle	76
Skin	72
Liver	68
Bone	22
Adipose tissue	10

Table 85.3 Water content as a percentage of total body weight

Age (years)	Males (%)	Females (%)
10–15	60	57
15–40	60	50
40–60	55	47
> 60	50	45

Total body water is commonly divided into two volumes, the extracellular fluid (ECF) volume and the intracellular fluid (ICF) volume.² Sodium balance regulates the ECF volume, whereas water balance regulates the ICF volume. Sodium excretion is normally regulated by various hormonal and physical ECF volume sensors, whereas water balance is normally regulated by hypothalamic osmolar sensors.⁴

EXTRACELLULAR FLUID

ECF is defined as all body water external to the cell, and is commonly subdivided into plasma and interstitial fluid volumes. The ECF is normally 40% of total body water and 25% of total body weight. With acute or chronic illness, ICF volume is reduced, and ECF volume is increased and may even exceed the ICF volume. The ECF volume can be divided into the plasma volume, the extracellular fluid volume, and the interstitial volume.

INTRACELLULAR FLUID

ICF is defined as all the body water within cells and, unlike the ECF compartment, is an inhomogeneous, multicompartmental entity, with different pH and ionic composition depending upon the organ or tissue being considered. The ICF volume is often determined by inference from the difference in measurements of the total body water and ECF spaces. This estimation suffers from the inaccuracies inherent in both ECF and total body water measurements. In general, the ICF is considered to be 60% of total body water and 35% of total body weight.

TRANSCELLULAR FLUID

Fluids in this compartment have a common characteristic of being formed by transport activity of cells. The fluid is extracellular in nature and will be considered as part of the interstitial volume. It may vary from 1 to 10 l, with larger volumes occurring in diseased states (e.g. bowel obstruction or cirrhosis with ascites), and is formed at the expense of the remaining interstitial and plasma volumes.

WATER METABOLISM

Water balance is maintained by altering the intake and excretion of water. Intake is controlled by thirst, whereas excretion is controlled by the renal action of antidiuretic hormone (ADH). In health, plasma osmolalities of about 280 mOsm/kg suppress plasma ADH to concentrations low enough to permit maximum urinary dilution.⁵ Above this value, an increase in ECF tonicity of about 1–2% or a decrease in total body water of 1–2 l, causes the posterior pituitary to release ADH, which acts upon the distal nephron to increase water reabsorption. Maximum plasma ADH concentrations are reached at an osmolality of 295 mOsm/kg.⁵ The osmotic stimulation also changes thirst sensation and, in the conscious ambulant individual, initiates water repletion (drinking), which is more important in preventing dehydration than ADH secretion and action. Thus, in health, the upper limit of the body osmolality (and therefore serum sodium) is determined by the osmotic threshold for thirst, whereas the lower limit is determined by the osmotic threshold for ADH release.⁶

Increase in osmolality caused by permeant solutes (e.g. urea) does not stimulate ADH release. ADH may also be released in response to hypovolaemia and hypotension, via stimulation of low and high pressure baroreceptors. ADH release is extremely marked when more than 30% of the intravascular volume is lost. ADH may also be stimulated by pain and nausea, which are thought to act through the baroreceptor pathways.⁴ ADH release may also be stimulated by a variety of pharmacological agents (Table 85.4). Renal response to ADH depends upon an intact distal nephron and collecting duct, and a hypertonic medullary interstitium. The capacity to conserve or excrete water also depends upon the osmolar load presented to the distal nephron.⁴

Table 85.4 Drugs affecting ADH secretion

Stimulate	Inhibit
Nicotine	Ethanol
Narcotics	Narcotic antagonists
Vincristine	Phenytoin
Barbiturates
Cyclophosphamide
Chlorpropamide
Clofibrate
Carbamazepine
Amitriptylline

WATER REQUIREMENTS

Water is needed to eliminate the daily solute load, and to replace daily insensible fluid loss (Table 85.5). With a normal daily excretion of 600 mOsm solute, maximal and minimal secretions of ADH will cause urine osmolality to vary from 1200 to 30 mOsm/kg respectively, and the urine output to vary from 500 ml to 20 l/day respectively. Skin and lung water losses vary, and may range from 500 ml to 8 l/day depending on physical activity, ambient temperature and humidity.

Table 85.5 Daily fluid balance (for a 70-kg man at rest in a temperate climate)

DISORDERS OF OSMOLALITY

ELECTROLYTES

Chemical compounds in solution may either:

• Remain intact (i.e. undissociated), in which case they are called non-electrolytes (e.g. glucose, urea)

• Dissociate to form ions, in which case they are called electrolytes. Ions carry an electrical charge (e.g. Na⁺, Cl⁻). Ions with a positive charge are attracted to a negative electrode or cathode, and hence are called ‘cations’. Conversely, ions with a negative charge travel towards a positive electrode or anode and are called ‘anions’. Each body water compartment contains electrolytes with different composition and concentration (Table 85.6)

Table 85.6 Electrolyte composition of body fluid compartments

SODIUM

Sodium is the principal cation of the ECF and accounts for 86% of the ECF osmolality. In a 70-kg man, total body sodium content is 4000 mmol (58 mmol/kg) and is divided into a number of compartments (Table 85.7). ECF concentration of sodium varies between 134 and 146 mmol/l. The intracellular sodium concentration varies between different tissues, and ranges from 3 to 20 mmol/l.

Table 85.7 The sodium compartments in a 70-kg man

	Total (mmol)	(mmol/kg)
Total body sodium	4000	58
Non-exchangeable bone sodium	1200	17
Exchangeable sodium	2800	40
Intracellular sodium	250	3
Extracellular sodium	2400	35
Exchangeable bone sodium	150	2

The standard Western society dietary sodium intake is about 150 mmol/day, but the daily intake of sodium varies widely, with urinary losses ranging from < 1 to > 240 mmol/day.⁷ Sodium balance is influenced by renal hormonal and ECF physical characteristics. The complete renal adjustment to an altered sodium load usually requires 3–4 days before balance is restored.

HYPONATRAEMIA

Hyponatraemia is defined as a serum sodium less than 135 mmol/l and may be classified as isotonic, hypertonic or hypotonic, depending upon the measured serum osmolality (Table 85.8).

Table 85.8 Common causes of hyponatraemia

Isotonic hyponatraemia

Plasma normally contains 93% water and 7% solids (5.5% proteins, 1% salts and 0.5% lipids). If the solid phase is elevated significantly (e.g. in hyperlipidaemia or hyperproteinaemia), any device which dilutes a specific amount of plasma for analysis will give falsely lower values for all measured compounds. This effect produces ‘factitious hyponatraemia’ and is associated with a normal measured serum osmolality.⁸ Measurement of plasma sodium by an ion-selective electrode is not affected by the volume of plasma ‘solids’ and therefore ‘pseudohyponatraemia’ will not occur with this method.⁸

Hypertonic hyponatraemia

In patients who have hypertonicity due to increased amounts of impermeant solutes (e.g. glucose, mannitol, glycerol or sorbitol), a shift of water from the ICF to the ECF occurs to provide osmotic equilibration, thus diluting the ECF sodium. Such resultant hyponatraemia is often associated with an increased measured osmolality. For example, in the presence of hyperglycaemia, for every 3 mmol/l rise in glucose, the serum sodium decreases by 1 mmol/l.⁹

Hypotonic hyponatraemia

Hyponatraemia is almost always caused by an excess of total body water, due to excessive hypotonic or water-generating i.v. fluids (e.g. 1.5% glycine, 0.45% saline or 5% glucose) or excessive ingestion of water, particularly in the presence of high circulating ADH concentrations. It may rarely be caused by loss of exchangeable sodium or potassium. In the latter circumstances, a loss of approximately 40 mmol of sodium or potassium, without a change in total body water content, is required to lower the serum sodium by 1 mmol/l. As hyponatraemia may be associated with an alteration in both total body water and total body sodium, the ECF may be increased (hypervolaemia), decreased (hypovolaemia) or exhibit no change (isovolaemia).⁵

In health, a fluid intake up to 15–20 l may be tolerated before water is retained and hyponatraemia occurs. In psychogenic polydipsia, if the water intake exceeds the renal capacity to form dilute urine, water retention and hyponatraemia will occur. With this disorder, the plasma osmolality exceeds urine osmolality. In circumstances where ADH is increased (e.g. hypovolaemia, hypotension, pain or nausea), or where renal response to ADH is altered (i.e. in renal, hepatic, pituitary, adrenal or thyroid failure), water retention occurs with lower intakes of fluid.

Transurethral resection of prostate (TURP) syndrome

Clinical features

The TURP syndrome consists of hyponatraemia, cardiovascular disturbances (hypertension, hypotension, bradycardia), an altered state of consciousness (agitation, confusion, nausea, vomiting, myoclonic and generalised seizures) and, when using glycine solutions, transient visual disturbances of blurred vision, blindness and fixed dilated pupils, following TURP. It has also been described following endometrial ablation.¹⁰ It may occurwithin 15 minutes or be delayed for up to 24 hours postoperatively,¹¹ and is usually caused by an excess absorption of the irrigating fluid which contains 1.5% glycine with an osmolality of 200 mosm/kg. Hyponatraemic syndromes have also been described when irrigating solutions containing 3% mannitol or 3% sorbitol have been used. Symptomatology usually occurs when > 1 l of 1.5% glycine or > 2–3 l of 3% mannitol or sorbitol are absorbed.¹²

The excess absorption of irrigating fluid causes an increase in total body water (which is often associated with only a small decrease in plasma osmolality), hyponatraemia (as glycine, sorbitol or mannitol reduces the sodium component of ECF osmolality) and an increase in the osmolar gap.^12,¹³ When glycine is used, other features include hyperglycinaemia (up to 20 mmol/l; normal plasma glycine concentrations range from 0.15 to 0.3 mmol/l), hyperserinaemia (as serine is a major metabolite of glycine), hyperammonaemia (following deamination of glycine and serine), metabolic acidosis and hypocalcaemia (due to the glycine metabolites glyoxylic acid and oxalate). Because glycine is an inhibitory neurotransmitter, and as it passes freely into the intracellular compartment when glycine solutions are used, hyperglycinaemia may be more important in the pathophysiology of this disorder than a reduction in body fluid osmolality and cerebral oedema.¹⁴