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Perioperative Electrolyte and Fluid Balance CEACCP 2005
Perioperative Electrolyte and Fluid Balance CEACCP 2005
fluid balance
Sahir S Rassam MB ChB MSc FFARCSI
David J Counsell MB ChB FRCA
solutes (i.e. Naþ and Cl). Because changes in Cl are mainly Electrolyte balance and clinical
secondary to changes in Naþ, the amount of Naþ in the ECF is implications
the most important determinant of ECF volume; thus, the mech-
anisms that control Naþ balance are the major mechanisms Sodium
defending ECF volume. However, the need to ensure optimal Sodium balance is related to ECF volume and water balance; daily
circulating volume is paramount and volume stimuli can ingestion has a wide range (50–300 mmol). It is regulated by the
override the osmotic regulation of vasopressin secretion. A rise kidneys in which the volume and constitution of filtrate reaching
in ECF volume inhibits vasopressin secretion, and a decline in the collecting ducts is dependent on GFR, sympathetic tone and
ECF volume increases its secretion. In addition, expansion of angiotensin II acting via the effects of ADH and aldosterone
ECF volume increases the secretion of natriuretic hormones, to conserve water and sodium (see above). Normothermic
the most important being secretion of atrial natriuretic peptide extra-renal losses are minimal (10 mmol day1).
(ANP) by the heart causing natriuresis and diuresis.2 Hypernatraemia leads to pyrexia, nausea, vomiting, convul-
sions, coma and focal neurological signs. Correction is advisable
Thirst and osmolality over 48–72 h with 5% dextrose. In hyponatraemia, symptoms
158 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 5 Number 5 2005
Perioperative electrolyte and fluid balance
The reverse occurs when the blood reaches the lungs. In respirat- underestimated and excess losses, both surgical and third-space
ory disturbances (acidosis or alkalosis), 30% of an acid load can losses, persist into the early postoperative period. Therefore, a
be buffered by such shifts between the ICF and ECF.4 general tendency towards hypovolaemia is usually present leading
It is important to recognise the clinical implication of excessive to thirst and vasopressin secretion.
use of chloride (normal saline) in fluid resuscitation. According There are two main components to the stress response to
to Stewart,5 the major determinant to Hþ concentration is the surgery: the neuroendocrine response and the cytokine response.7
strong ion difference (SID) in the body. A normal SID (42–46 The neuroendocrine response is stimulated initially by painful
mmol litre1) is obtained by adding together the concentrations afferent neural stimuli reaching the CNS. It may be diminished
of the main cations in solution (Naþ, Kþ, Ca2þ, Mg2þ) and by dense neural blockade from regional anaesthesia. The cytokine
subtracting the concentrations of the main cations (Cl, lactate). response is stimulated by local tissue damage at the site of
A decrease in SID is associated with a metabolic acidosis and this surgery itself (the more extensive the surgery the higher the
can be precipitated by large volume of saline because renal excre- response) and is independent of neural blockade.
tion of Naþ occurs in preference to Cl and Hþ. The cause of The most important response to anaesthesia and surgery in the
metabolic acidosis may be erroneously attributed to tissue hypo- perioperative period is sodium and water retention. In general,
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 5 Number 5 2005 159
Perioperative electrolyte and fluid balance
Cause
Hypernatraemia Salt gain: salt ingestion, Water depletion: diabetes Naþ retention owing to corticosteroid
Naþ >150 mmol litre1 excessive i.v. administration insipidus, chronic renal failure, osmotic excess
diuresis, fever, hyperventilation,
decrease water intake, vomiting,
diarrhoea or sweating
Hyponatraemia Decrease intake, insufficient Water retention: cardiac, hepatic, nephrotic. Diuretic therapy, hypoadrenalism, salt
Naþ <135 mmol litre1 sodium during i.v. fluid therapy SIADH (syndrome of inappropriate ADH losing nephropathy, renal tubular
release), drugs, postoperative stress acidosis. Extrarenal: diarrhoea,
vomiting, third-space losses
Hyperkalaemia Blood transfusion, excessive i.v. Release from cells: burns, rhabdomyolysis, Impaired excretion: renal failure,
Kþ >5 mmol litre1 administration intravascular haemolysis, suxamethonium Addison’s disease, potassium
sparing diuretics
this situation to maintain circulatory volume and adequate organ hepatic or renal (nephrotic) and urine sodium is usually <20 mmol
perfusion. litre1. However, if hyponatraemia is associated with normo-
volaemia, the most common causes are SIADH (syndrome of
Urine biochemistry and diagnosis of inappropriate ADH release), postoperative stress, drugs and
electrolytes abnormalities renal failure; plasma osmolality is usually decreased and fluid
restriction is required.1
The aetiology of important electrolyte disturbances is summarized
in Table 2. Measurement of urine and plasma osmolalities and
urine volume helps in the diagnosis. References
1. Aitkenhead AR, Rowbotham DJ, Smith G. Textbook of Anaesthesia, 4th Edn.
Hypernatraemia London: Churchill Livingstone, 2001
If urine output is low and urine osmolality high, then both ADH 2. Ganong WF. Review of Medical Physiology, 19th Edn. Stamford: Appleton &
Lange, 2000
secretion and the renal response to it are present. The cause here is
3. Dobb GB. Body water, electrolytes and parenteral fluid therapy.
most likely extrarenal water loss. If both urine output and urine
In: Churchill-Davidson HC ed. A Practice of Anaesthesia. Chicago: Lloyd-
osmolality are high, then osmotic diuresis is suspected. If urine Luke (Medical Books) Ltd, 1984; 568–86
osmolality is less than plasma osmolality, then the cause is attrib- 4. Maloney DG, Appadurai IR, Vaughan RS. Anions and the anaesthetist.
utable to reduced ADH secretion or abnormal renal response to Anaesthesia 2002; 57: 140–54
ADH; in both cases, urine output is high.1 5. Stewart PA. Modern quantitative acid–base chemistry. Can J Physiology
Pharmacol 1983; 61: 1444–6
Hyponatraemia 6. Scheingraber S, Rehm M, Sehmisch C, Finsterer U. Rapid saline infusion
produces hyperchloremic acidosis in patients undergoing gynaecologic
If hypovolaemia is present, then the loss is either renal (urine surgery. Anesthesiology 1999; 90: 1265–70
sodium >20 mmol litre1) or extrarenal (urine sodium 7. Desborough JP. The stress response to trauma and surgery. Br J Anaesth
<15 mmol litre1); in these conditions, saline is required. If 2000; 85: 109–17
hypervolaemia (oedema) is present, the cause could be cardiac, See multiple choice questions 119–122
160 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 5 Number 5 2005