When inorganic salts are in solution, as in the extracellular or intracellular fluids of the body, they dissociate into ions. Ions are of two kinds: (1) cations, which are electropositive; and (2) anions, which are electronegative: collectively these are the electrolytes. The most accurate way of describing the chemical concentrations, reactivity and osmotic power of these ions is in SI units as millimoles per litre (mmol/litre). The cations include sodium, potassium, calcium and magnesium; the anions include chloride, phosphate, bicarbonate and sulphate. The distribution of the salts within the fluid compartments of the body controls the passage of water through the cell walls and maintains acid—base equilibrium.
Sodium is the principal cation content of the extracellular fluid. The total body sodium amounts to approximately 5000 mmol, of which 44 per cent is in the extracellular fluid, 9 per cent in the intracellular fluid and the remaining 47 per cent in bone. The sodium housed in bone merits special notice: a little more than half of it is osmotically inactive and requires acid for its solution; the remainder is water soluble and exchangeable. Thus, there is a large storehouse of sodium ready to compensate abnormal loss from the body. The daily intake of sodium is inconstant. On average it is 1 mmol/kg sodium chloride or 500 ml of isotonic 0.9 per cent saline solution. An equivalent amount is excreted daily, mainly in the urine and some in the faeces. The loss in perspiration normally is negligible; however, in people not acclimatized to tropical heat, prolonged profuse sweating results in a considerable loss of sodium — as much as 85 mmol/hour. If water alone is given to counter-balance the fluid loss, serious sodium depletion can occur from excessive sweating. (See also mucoviscidosis, in Chapter 54 of this book on ‘The gallbladder and bile ducts’.)
Control by adrenal corticoids
The output of sodium, governed by the variation in the avidity with which the renal tubules reabsorb sodium from the glomerular filtrate and the amount of sodium excreted by the sweat glands, is under the control of the adrenal corticoids, the most powerful conservator of sodium being aldosterone. When the adrenal glands have been destroyed by disease or extirpated, there is an unbridled loss of sodium in the urine.
The sodium excretion shut down of trauma
Following trauma/surgery there is a variable period of reduced excretion of sodium. For this reason it may be inadvisable to administer large quantities of isotonic (0.9 per cent) saline solution after an operation. The period of sodium excretion shut down can last for up to 48 hours and is due to increased adrenocortical activity.
Sodium depletion (syn. hyponatraemia)
The most frequent cause of sodium depletion seen in surgical practice is obstruction of the small intestine, with its rapid loss of gastric, biliary, pancreatic and intestinal secretions by antiperistalsis and ejection, whether by vomiting or aspiration. Duodenal, total biliary, pancreatic and high intestinal external fistulae also are all notorious for bringing about early and profound hyponatraemia. Severe diarrhoea due to dysentery, cholera, ulcerative colitis or pseudomembranous colitis will cause hyponatraemia with acidosis. The finding of hyponatraemia with elevated potassium would suggest adrenocortical insufficiency. Hyponatraemia is also seen in SIADH.
There is one other less obvious, and surreptitious, means whereby the patient is robbed of sodium and that is by gastric aspiration combined with allowing the patient to drink as he or she pleases and promptly aspirating the fluid swallowed. The act of drinking excites the flow of gastric juice, and this is also aspirated. During this form of therapy, should the patient be receiving intravenous dextrose solution to maintain fluid balance, he or she will soon become a victim of hyponatraemia.
Clinical features. Clinical features of hyponatraemia with salt and water depletion are due to extracellular dehydration. In established cases the eyes are sunken and the face is drawn. In infants the anterior fontanelle is depressed. The tongue is coated and dry; in advanced cases it is brown in colour. Unlike the dehydration produced by loss of water only, in water and salt depletion thirst is not particularly in evidence. The skin is dry and often wrinkled, making the patient look older than his or her years. The subcutaneous tissue feels lax. Peripheral veins are contracted and contain dark blood. The arterial blood pressure is likely to be below normal. The urine is scanty, dark in colour, of a high specific gravity and, except in cases of salt-losing nephritis, contains little or no chloride.
Presuming that the haemoglobin level before the dehydration commenced was normal, the haematocrit reading (PCV) provides an index of the degree of haemoconcentration. However, haemoconcentrations can be masked by preexisting anaemia. Laboratory investigations would show normal or slightly reduced serum sodium with low urinary output and low urinary sodium.
Hyponatraemia with a normal or increased extracellular fluid volume arises as a result of too prolonged administration of a sodium-free solution (cf. Water intoxication, above).
Sodium excess (syn. hypernatraemia)
This is likely to arise if a patient is given an excessive amount of 0.9 per cent saline solution intravenously during the early postoperative period when, as has been described, some degree of sodium retention is to be expected. The result is an overloading of the circulation with salt and its accompanying water.
Clinical features. Slight puffiness of the face is the only early sign. The patient makes no complaint. Pitting oedema should be sought, especially in the sacral region, but for pitting oedema to be present at least 4.5litres of excess fluid must have accumulated in the tissue spaces. The patient’s weight increases pan passu with the water-logging. Signs of overhydration in infancy (infants are very susceptible) are increased tension in the anterior fontanelle, increased weight, an increase in the number of urinations and oedema.
Potassium is almost entirely intracellular. No less than 98 per cent is intracellular, and only 2 per cent is present in the extracellular fluid. Three quarters of the total body potassium (approximately 3500 mmol) is found in skeletal muscles. When the body needs endogenous protein as a source of energy, potassium, as well as nitrogen, is mobilised. The mobilised potassium passes to the extracellular fluid, but the surplus over and above the normal content is so rapidly excreted by healthy kidneys that the concentration of potassium in the serum remains unaltered. Each day a normal adult ingests approximately 1.0 mmol/kg of potassium in food; fruit, milk and honey are rich in this cation. Except for a very small quantity in formed faeces, and a still smaller quantity in sweat, an amount corresponding to the intake is excreted in the urine.
The augmented potassium excretion of trauma. Following trauma, including operation trauma, there is a spell, varying directly with the degree of tissue damage, of increased excretion of potassium by the kidneys. This loss is greatest during the first 24 hours and lasts, for example in the case of partial gastrectomy, for about 3 or 4 days. So great are the body’s reserves of potassium that, unless the patient was severely depleted at the time of the operation, hypokalaemia may not reveal itself for 48 hours. However, potassium is such a key intracellular cation that carefully monitored replacement should start early in the postoperative period in all patients, with the exception of those that have evidence of renal dysfunction.
Hypokalaemia. Hypokalaemia can occur suddenly or gradually.
Sudden hypokalaemia is unlikely to be encountered in surgical practice. It occurs most frequently in diabetic coma treated by insulin and prolonged infusion of saline solution.
Gradual hypokalaemiais the type encountered in surgical practice. It is most commonly seen in patients who present for surgery with chronic hypokalaemia as a result of potassium-losing medications such as diuretics. The diarrhoea from ulcerative colitis, villous tumours of the rectum (see Chapter 59 of this book on ‘The vermiform appendix’) and the loss from external fistulae of the alimentary tract are also common causes (e.g. duodenal fistula, ileostomy); the potassium content of the discharge from some of these fistulae is twice that of the plasma potassium concentration. Another frequent cause of hypokalaemia is prolonged gastroduodenal aspiration with fluid replacement by intravenous isotonic saline solution. It is also prone to occur in the postoperative period following extensive resections for carcinoma of the alimentary tract, because often the operation has to be undertaken after months of weight loss and potassium depletion.
Most patients are asymptomatic, but at risk of the sequelae of hypokalaemia such as cardiac arrythmias. Such consequences are more likely during surgery and anaesthesia, especially in the presence of pre-existing myocardial disease. Symptoms of severe hypokalaemia include listlessness and slurred speach, muscular hypotonia, depressed reflexes and abdominal distension as a result of a paralytic ileus. Weakness of the respiratory muscles may result in rapid, shallow, gasping respirations; these are conducive to postoperative pulmonary complications. The diagnosis is supported by electrocardiography (ECG), which may. show a prolonged QT interval, depression of the ST segment and flattening or inversion of the T-wave.
Oral potassium. Potassium can be given in the form of milk, meat extracts, fruit juices and honey. However, in hospital practice, effervescent tablets of potassium chloride 2 g can be given by mouth 6-hourly.
Intravenous potassium. Rapid intravenous supplementation (especially when renal function is impaired) carries the risk of dysrhythmias and cardiac arrest if the serum concentration rises to a dangerous level. Administration should be properly controlled; the level of potassium should be checked daily; the urine output must be adequate. When there is no associated alkalosis, the potassium deficit can be restored by adding 40 mmol potassium chloride to each litre of 5per cent glucose, glucose—saline or 0.9 per cent saline solution, which is given 6—8-hourly. Severe hypokalaemia should be treated in a high dependency or intensive care environment.
For hypokalaemic alkalosis see later.
Estimation of electrolyte balance
Sodium, with its equivalent anions, accounts for about 90 per cent of the osmotic pressure of the plasma. Changes in the sodium content coincide with changes in the osmolality of all the body fluids. The serum sodium value is normally between 137 and 147 mmol /litre. Whenever possible, the serum chloride and bicarbonateshould be estimated simultaneously because variations in the one may be accompanied by opposite changes in the other. The normal level of chloride is 95—105 mmol/litre, and of bicarbonate 25—3 0 mmol /litre; the sum of the two remains roughly constant at 120—135 mmol/litre.
Potassium deficiency is present if the serum potassium value is less than 3.5 mmol/litre. The normal range is 3.5—5.0 mmol/litre. It must be remembered that intracellular potassium deficiency may be present although the plasma concentration is normal, and that deficiency is to be expected if oral feeding has been withheld for more than 4 days. Estimation of potassium in the urine or aspirated gastrointestinal contents serves as a guide to the rate of depletion and the replacement necessary.
Calcium is an extracellular cation with a plasma concentration of 2.2—2.5 mmol/litre. It exists in three forms: bound to protein, free nonionised and free ionised — the last form being the component necessary for blood coagulation and affecting neuromuscular excitability. The ionised proportion falls with increasing PH; thus in respiratory alkalosis due to hyperventilation there may be tetany — with an apparently normal total serum calcium level. In the urine, the ionisation and the solubility of calcium are similarly depressed if the pH is elevated, thus promoting stone formation. The serum level of calcium is likely to be modified by any factor promoting or inhibiting its absorption from the bowel, its storage in bone or its elimination by the kidneys: such factors include vitamin D and phytic acid, parathormone and calcitonin (see Chapter 44), and the state of renal and small-bowel function.
The management of abnormal calcium blood levels depends, where possible, on removal of the cause, for example removal of a parathyroid tumour (see Chapter 44), or in the coagulation disorder due to massive transfusion of blood containing acid citrate dextrose (ACD, see below), 10 ml of 10 per cent calcium gluconate may be injected slowly intravenously. If oral administration is possible, calcium aspirin is useful (see Chapter 44). On a long-term basis, the diet should be adjusted to provide a high calcium and a low phosphate intake.
Magnesium is an intracellular cation which shares some of the properties of potassium and some of calcium. The normal magnesium concentration is 0.7—0.9 mmol /litre. The average daily intake is approximately 10 mmol. Magnesium deficiency may occur when there is prolonged loss of gastrointestinal secretions due to fistulae or ulcerative colitis, very prolonged administration of intravenous fluids without magnesium supplements, following massive small bowel resections, and in some cases of cirrhosis of the liver or disease of the parathyroids. The clinical picture of magnesium deficiency is marked by central nervous system irritability, ECG changes, lowered blood pressure and lowered protein synthesis. Postoperative cardiac arrythmias (e.g. de novo atrial fibrillation) are commonly associated with both hypokalaemia and hypomagnesaemia.
Treatment. For the treatment of mild hypomagnesaemia 20 mmol as magnesium sulphate can be added to 5percent-dextrose or normal saline over a 24-hour period. Magnesium supplements are essential in hyperalimentation.