Water, electrolyte and acid-base balance

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11 Water, electrolyte and acid-base balance

Chapter Contents

Introduction 367
Salt and volume distribution 367
Sodium 370
Potassium 375
Magnesium 378
Phosphate 379
Acid–base disorders 380

Introduction

The human body is mainly water. Total body water in litres is calculated as 0.6 × weight (kg) in men, and 0.5 × weight (kg) in women. Water is compartmentalized in the body, two-thirds within the intracellular space and one-third as extracellular fluid (ECF) (of which one-third is plasma and two-thirds are in the interstitial space).

Osmotic pressure maintains the tonicity of any compartment:

• Within cells, K+ determines osmotic pressure confined by the hydrophobic cell membrane.
• Within the extracellular space, Na+ acts as the principle osmotic determinant. Intravascular protein, as well as Na+, allows plasma (separated by relatively permeable capillary walls) to maintain an osmotic gradient against tissue.

Salt and volume distribution

Na+ retention and excretion control extracellular volume (water will passively follow salt). Systemic baro-receptors (carotid sinus, aortic arch) ‘sense’ changes in arterial tone (a function of cardiac output and systemic vascular resistance). A fall in effective arterial blood volume (EABV) activates the sympathetic nervous system, leading to Na+ retention by the kidney. With an expanded EABV, increased renal Na+ loss occurs.

Oedema

Oedema is a clinically noticeable increase in the interstitial component of the ECF (apparent after > 2 L fluid gain, obvious in dependent areas such as the ankles). For this to occur, salt and water must be retained and capillary permeability permits fluid shifts into the interstitium, e.g. in acute kidney injury.

Any cause of a fall in EABV leads to salt and water retention through the activation of the renin–angiotensin–aldosterone system and this releases antidiuretic hormone (ADH, vasopressin). If prolonged, over time this net gain in sodium and water presents as oedema, e.g. in heart failure and hepatic cirrhosis. This mechanism plays a bigger role than a fall in intravascular oncotic pressure (if plasma proteins such as albumin are reduced, e.g. in the nephrotic syndrome), leading to water loss into the interstitium. Endothelial dysfunction, or ‘leaky capillaries’, is often present in addition to falling arterial tone.

Water and volume

• Hypothalamic osmoreceptors, which sense osmolality rather than volume, increase thirst, and pituitary ADH release in response to falling total body water (TBW). ADH regulates free water absorption in the renal collecting ducts to reverse this.
• With water overload (and a falling osmolality), thirst and ADH release are suppressed, with dilute urine being passed.
• For normal water homeostasis, the body requires a normal hypothalamus, access to water, a functioning pituitary (ADH release) and responsive collecting ducts.

Assessing volume status

Thirst is a symptom of dehydration; oedema indicates increased volume.

• Examine pulse rate and BP, both lying and standing; a postural drop in BP is a good indicator of hypovolaemia.
• The JVP is helpful; it is high in increased circulating volume and low in decreased volume.
• A fluid challenge done accurately by yourself gives accurate information with a central vein catheter in place (Fig. 11.1).
• Daily weights and assessment of peripheral perfusion are also helpful in assessing volume status.
• Re-assess frequently and get a CXR for further evidence of fluid overload. Treatment of oedema is discussed under renal disease (p. 334), hepatic cirrhosis (p. 188) and heart failure (p. 426).
image

Fig. 11.1 The effects of rapid administration of a ‘fluid challenge’ to patients with a central venous pressure (CVP) within the normal range

(Based upon Sykes MK 1963).

Fluid therapy in hospital

Two common circumstances necessitate fluids as therapy (Table 11.1) in hospital:

• Patients who cannot drink for any reason require maintenance fluids. This may be given by intravenous infusion (IVI) for short periods, but use the enteral route if possible. If fluids are required for > 5 days, a naso-gastric tube with water and/or enteral nutrition provides more physiological replacement than IV fluids.
• Patients who are dehydrated or hypovolaemic require replacement or resuscitation fluid, usually intravenously. Always check patients’ renal and cardiac function before prescribing a fluid regimen.

Table 11.1 IV fluids in general use for fluid and electrolyte disturbances

image

The volume administered varies according to the state of hydration; in otherwise well ‘nil by mouth’ patients with no losses, aim for 2 L/24 hours of saline (0.18%) and glucose (4%), usually with added potassium 20 mmol/L. Post-surgical fluid therapy should reflect the nature of the surgery (and the likely ongoing losses).

Sodium

Disorders of sodium are more accurately disorders of water than of sodium, as disturbances of sodium concentration are mainly caused by a disturbance of water balance. The danger posed by a low or high serum Na+ comes from both the electrolyte abnormality and its correction; the skull does not allow the brain to change in volume, so movement of water into the CNS risks increased intracranial pressure (and eventually tentorial herniation). Equally, movement of water out of the brain can lead to sudden and irreversible osmotic injury (central pontine myelinolysis (CPM)).

Hyponatraemia

Hyponatraemia (plasma Na+ < 135 mmol/L) is common in hospitalized patients, but symptomatic hyponatraemia is very much less common — and more dangerous.

Clinical features

Clinical features of hyponatraemia are due to cerebral swelling, and include headaches, apathy, and confusion progressing to coma and seizures (encephalopathy). These tend to occur with a serum sodium of:

• <125 mmol/L if acute (< 48 hours, usually post-operative) or
• <110 mmol/L if chronic

Certain patients are more at risk for the neurological complications of hyponatraemia: the elderly, malnourished or alcoholic patients, pre-menopausal women (oestrogen may enhance the body’s response to ADH) and those whose hyponatraemia is caused by thiazide diuretic use.

Always exclude pseudohyponatraemia. Around 93% of plasma is water; conditions that increase the 7% of plasma made up of protein and lipids (e.g. hyperlipidaemia, hyperglycaemia, myeloma proteins) artefactually reduce the water phase in which Na+ is assayed, falsely reducing the measured sodium.

Investigations

• Repeat serum Na+, K+, HCO3− and glucose.
• Measure/calculate blood and urine osmolality.
• Perform renal, adrenal and thyroid function tests.
• Assess volume status (p. 368). Hyponatraemia with a normal, decreased or increased extracellular volume has different causes and different therapy (Fig. 11.2).
image

Fig. 11.2 Diagnosis and causes of hyponatraemia.

Hyponatraemia with a normal extracellular volume

Excess body water results from an abnormally high intake.

• Excessive use of 5% glucose IV infusions without sodium is the commonest situation in hospital.
• Absorption of sodium-free bladder irrigation fluid after prostatectomy is another possible cause.
• Psychogenic polydipsia occurs usually in psychiatric patients who drink > 12 L a day (above the renal excretion capacity).
• The syndrome of inappropriate antidiuretic hormone secretion (SIADH) Where hypotonic fluid administration has been excluded, the syndrome of inappropriate anti-diuretic hormone secretion (SIADH) is the commonest cause. It produces a hyponatraemia, normal or slightly increased extracellular volume, and a low plasma osmolality with an inappropriately high urine osmolality (> 100 mosm/kg). Urine sodium excretion > 30 mmol/L continues because of the release of atrio-natriuretic peptide due to increased volume. This syndrome occurs because there is inappropriate secretion of ADH from the posterior pituitary or an ectopic source, resulting in renal free water excretion. Renal, adrenal and thyroid function is normal. Common causes of SIADH include tumours (e.g. small cell carcinoma of the lung), pulmonary disorders (e.g. pneumonia), neurological causes (e.g. meningitis) and drugs (e.g. phenothiazine).
• Other causes where ADH secretion occurs inappropriately include:

• Adrenal failure. This causes cortisol deficiency, which leads to an increased secretion of ADH and decreased mineralocorticoids which cause hyponatraemia.
• Hypothyroidism. Hyponatraemia in hypothyroidism is due to ADH secretion caused by a decreased cardiac output and glomerular filtration rate.
• Drugs. Many drugs cause hyponatraemia due to ADH release (antipsychotics, tricyclics, carbamazepine, antineoplastics, narcotics). Some drugs, e.g. NSAIDs, chlorpropamide, potentiate the antidiuretic action of vasopressin. Stress, e.g. post-surgical, also causes vasopressin release.

•General principles of management

• Stop drugs and hypotonic IV fluids that are contributing to hyponatraemia.
• Restrict fluid to < 1 L/day.
• Correct hypokalaemia and/or hypomagnesaemia (if present); correction improves renal handling of salt and water.

•Treating hyponatraemia without encephalopathy

• Give oral NaCl 40–80 mmol/day with/without furosemide 20–40 mg/daily.
• Asymptomatic proven SIADH may be treated with demeclocycline 150–300 mg 6-hourly (causes nephrogenic diabetes insipidus and free water loss).
• Aquaretics (V2 receptor antagonists blocking ADH’s action), e.g. conivaptan, which produce a free water diuresis, are also being used.

•Treating hyponatraemia with encephalopathy, see Chapter 20, Emergencies in medicine, p. 711

• A serum Na+ rise of 5 mmol/L will almost always control seizures.
• Transfer to the HDU and ensure regular clinical review.
• Document neurology regularly.
• Repeat Na+ after 2 hours and then 4-hourly.
• If acute: aim to increase Na+ by 2 mmol/L/hour or until asymptomatic.
• If chronic: aim to increase Na+ by 0.5 mmol/L/hour or until asymptomatic.
• Never correct by > 10 mmol/L/24 hours. CPM often takes a few days to develop; it causes a spastic para-/quadriparesis and mental disturbances, and can lead to death. MRI is useful in diagnosis.
• Calculation:

image

• For practical purposes total body water can be calculated as 50% of weight in kg.
• 3% NaCl (hypertonic saline) contains 1 mmol NaCl per 2 mL (513 mmol in 1 L). Acute and chronic hyponatraemia require different hourly correction rates (see above)

For example, a 50 kg woman has a serum sodium of 115 mmol/L. She requires 10 mmol to correct to 125 mmol/L. Thus, 10 × half of the body (i.e. 25) = 250. Thus, she requires 250 mmol of 3% NaCl, which is 500 mL. This should be given slowly over 4–6 hours via a central vein.

Hyponatraemia with a decreased extracellular volume

A decreased volume stimulates thirst and vasopressin release, which in turn inhibits water excretion. Losses from the kidney occur in tubulointerstitial disease, the recovery phase of acute tubular necrosis, unilateral renal artery stenosis, excessive use of diuretics, adrenocortical insufficiency and osmotic diuresis (e.g. hyperglycaemia, severe uraemia). Losses from the gastrointestinal tract are due to vomiting, diarrhoea, naso-gastric suction and haemorrhage (Table 11.2). Losses can also occur from the skin (burns), pericarditis and peritonitis.

• Management. The underlying diagnosis is usually apparent. Urinary Na+ will be very low (< 10 mmol/L) unless the sodium loss is renal in origin. Replace salt and water with oral rehydration fluid (p. 59) or IV 0.9% NaCl. If the patient is encephalopathic (depressed level of consciousness, fitting), hypertonic 3% sodium chloride is given slowly as above.

Table 11.2 Average concentrations and potential daily losses of water and electrolytes from the gut

image

Hyponatraemia with an increased extracellular volume

In this situation there is evidence of volume overload with a decreased circulatory volume, e.g. oedema. This leads to a reduced glomerular filtration rate with avid reabsorption of sodium from the proximal tubule. This in turn leads to a reduced delivery of chloride to the diluting ascending loop of Henle. There is thus an inability to excrete dilute urine.

• Causes include heart failure, liver cirrhosis and the nephrotic syndrome, in which there is evidence of fluid overload that exceeds the increase in sodium so that a dilutional hyponatraemia occurs.
• Management

• Fluid is restricted to < 1 L intake per day.
• A loop diuretic

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