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Fluid and electrolyte therapy

Chapter 85 Fluid and electrolyte therapy

Anthony Delaney, Simon Finfer

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

TONICITY
Osmolality is a measure of the number of osmol/kg water. The osmolality of the ECF is due largely to
sodium salts. Clinical effects of hyperosmolality, due to excess solute, depend upon whether the solute
distributes evenly throughout the total body water (e.g. permeant solutes of alcohol or urea) or distributes
in the ECF only (e.g. impermeant solutes of mannitol or glucose). With impermeant solutes,
hyperosmolality is associated with a shift of fluid from the ICF to the ECF compartment. Hyperosmolality
due to increased impermeant solutes is knownas hypertonicity. This condition may also be associated
with a reduction in the serum sodium concentration (see below).

WATER EXCESS
In a 70-kg man, for every 1 l excess water, ECF increases by 400 ml and ICF increases by 600 ml, on
average. The osmolality also decreases by 6–7 mOsm/kg and the serum sodium falls by 3.0–3.5 mmol/l.

WATER DEFICIENCY
In a 70-kg man, for every 1 l water loss, 600 ml is lost from the ICF and 400 ml from the ECF. The
osmolality also increases by 7–8 mOsm/kg and the serum sodium rises by 3.5–4.0 mmol/l.

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

1 Spurious result

Isotonic

Hyperlipidaemia

Hyperproteinaemia

Hypertonic

Hyperglycaemia

Mannitol, glycerol, glycine or sorbitol excess

2 Water retention

Renal failure

Hepatic failure

Cardiac failure

Syndrome of inappropriate ADH secretion

Drugs

Psychogenic polydipsia
 3 Water retention and salt depletion

Postoperative, post trauma or patients with excess fluid losses given inappropriate fluid replacement

Adrenocortical failure

Diuretic excess

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

Treatment
Treatment is largely supportive with the management of any reduction in plasma osmolality being based
on the measured plasma osmolality and not the plasma sodium. If the measured osmolality is > 260
mOsm/kg and mild neurological abnormalities exist, and if the patient is haemodynamically stable with
normal renal function, close observation and reassurance (e.g. the visual disturbances are reversible and
will last for less than 24 hours) are usually all that is needed. If the patient is hypotensive and bradycardic
with severe and unresolving neurological abnormalities, haemodialysis may be warranted. Hypertonic
saline is only used if the measured osmolality is < 260 mOsm/kg and severe non-visual neurological
abnormalities exist.15

Syndrome of inappropriate ADH secretion (SIADH)

This syndrome is a form of hyponatraemia in which there is an increased concentration of ADH
inappropriate to any osmotic or volume stimuli that normally affect ADH secretion. 16 Diagnostic criteria
and common causes are listed in Tables 85.9 and 85.10, respectively.
Table 85.9 Criteria for the diagnosis of syndrome of inappropriate antidiuretic hormone (SIADH)

Hypotonic hyponatraemia

Urine osmolality greater than plasma osmolality

Urine sodium excretion greater than 20 mmol/l

Normal renal, hepatic, cardiac, pituitary, adrenal and thyroid function

Absence of hypotension, hypovolaemia, oedema and drugs affecting ADH secretion

Correction by water restriction

Table 85.10 Aetiologies of syndrome of inappropriate antidiuretic hormone (SIADH)

Ectopic ADH production by tumours

Small cell bronchogenic carcinoma

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