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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2826_Библиотеки_им_академика_М_И_Перельмана.pdf
Body Fluid Compartments 323
Inspection and palpation are usually sufficient to identify oedema.
Compression of the skin of the affected area with a fingertip for 10 seconds
results in ‘pitting’. Localized oedema is most likely to result from a local
cause, e.g. venous obstruction. The location of generalized oedema, e.g. with
cardiac failure, renal or liver disease, is often most prominent in the legs
and feet in ambulatory patients and in the sacral region in those who are
confined to bed.
Intravenous fluids in clinical practice
Intravenous fluids are frequently used in hospital to maintain fluid balance
in patients unable to take fluids orally and to replenish substantial deficits or
continuing losses. Crystalloids, e.g. sodium chloride 0.9%, contain low molecular weight salts or sugars that dissolve completely in water and pass freely
between intravascular and interstitial compartments (Table 8.3). Glucose 5%
Table 8.3 Crystalloids in general use
Osmolarity
(mosmol/
kg)
Normal plasma
values
Sodium chloride 0.9%
Sodium chloride
Na+
K+
(mmol/
L)
Cl−
(mmol/L)
(mmol/
L)
142 4.5 103 285–295
154 – 154 308
31 – – 283
0.18%/glucose 4%
Glucose 5%
Hartmann’s
– – – 278
130 4 109 273
solution/Ringer’s
lactate solution
Plasma-Lyte® 148
1. Volume expansion in hypovolaemic patients. Rarely to maintain fluid balance when
there are large losses of sodium. Excessive sodium and chloride (compared to plasma)
may cause hypernatraemia and hyperchloraemic metabolic acidosis, respectively.
2. Maintenance of fluid balance in normovolaemic, normonatraemic patients.
3. To replace water. Only given alone when there is no significant loss of electrolytes. Also
may be alternated with sodium chloride 0.9% as an alternative to (2).
4. In fluid maintenance and replacement. Provides bicarbonate from metabolism of
lactate. Also contains calcium 2 mmol/L.
5. Fluid replacement (e.g. burns, fracture, infection), intraoperative fluid replacement.
*NB: In a normal adult 1.5–2.5 L (25–35 mL/kg/24 hours) of fluid containing about 70–100
mmol sodium and 40–80 mmol potassium are required to maintain balance. Fluids are given
with or without potassium chloride (depending on daily requirements and plasma levels) given
as ready-mixed bags in preference to adding potassium chloride concentrate to a bag.
140 5 98 295
Indication*
1
2
3
4
5
324 Water, electrolytes and acid–base balance
is essentially free water and distributes evenly across total body water
(i.e. across all three major fluid compartments) after intravenous administration;
very little remains in the intravascular space. Sodium chloride 0.9% remains
in the extracellular space and thus about one-third of the volume infused will
remain in the intravascular space. Colloids (e.g. dextran 70, gelatin) contain
larger molecular weight substances and remain in the intravascular space for a
longer period than crystalloids. Colloids are used to expand circulating volume in
haemorrhage (until blood becomes available), burns and sometimes septicaemia.
Although remaining in the intravascular space longer than crystalloids, comparative studies have not shown a definite advantage of colloids over crystalloids in
hypovolaemic patients. Side effects of colloids are hypersensitivity reactions
including anaphylactoid reactions and a transient increase in bleeding time.
Assessment and monitoring of fluid balance are made from the history
(e.g. vomiting, diarrhoea), clinical examination and observations (skin turgor,
capillary refill time, jugular venous pressure [JVP], pulse, lying and standing
blood pressure, urine output), fluid balance charts and daily weights. Invasive
cardiac monitoring is also used in critical care settings. Measurement of
central venous pressure before and after an intravenous fluid challenge is
used to assess volume status (p. 330).
In the UK, the National Institute for Health and Care Excellence (NICE)
has produced guidelines on intravenous fluid therapy in adults in hospital.
Intravenous fluid prescriptions should be reviewed daily. Prescriptions
must take into account all other sources of fluid and electrolyte intake,
including oral intake, drugs and blood products. Before intravenous fluids are
prescribed, clinical assessment should determine:
• The patient’s fluid and electrolyte needs
• Whether fluids are needed for resuscitation, maintenance (see Table 8.1), or
to replace a deficit, e.g. hypovolaemia as a result of diarrhoea and vomiting
• The type of fluid required
• The appropriate rate of fluid administration, the volume to be administered
and the likely duration that intravenous fluids will be required.
Suggestions for appropriate use of the different types of fluid are
indicated in Table 8.3.
REGULATION OF BODY FLUID HOMEOSTASIS
Maintenance of the effective circulating volume is essential for adequate
tissue perfusion and is mainly related to the regulation of sodium balance. In
contrast, maintenance of osmolality prevents changes in cell volume and is
largely related to the regulation of water balance.
Regulation of extracellular volume
The regulation of extracellular volume is determined by a tight control of the
balance of sodium, which is excreted by normal kidneys. Although only a
Regulation of Body Fluid Homeostasis 325
small proportion of total extracellular fluid resides in the arterial circulation,
it is the fullness of the arterial vascular compartment – or the so-called
effective arterial blood volume (EABV) – that is the primary determinant of
renal sodium and water excretion. The fullness of the arterial compartment
depends on a normal ratio between cardiac output and peripheral arterial
resistance. Thus diminished EABV is initiated by a fall in cardiac output or
a fall in peripheral arterial resistance (an increase in the holding capacity of
the arterial vascular tree). When the EABV is expanded, this in turn leads to
an increase in urinary sodium excretion and vice versa.
Two types of volume receptors sense changes in the EABV:
• Extrarenal: in the large vessels near the heart
• Intrarenal: in the afferent renal arteriole, which controls the renin–
angiotensin system via the juxtaglomerular apparatus.
A decrease in effective circulating volume leads to activation of these
volume receptors, which in turn leads to an increase in sodium (and
hence water) reabsorption by the kidney and expansion of the extracellular
volumevia stimulation of the sympathetic nervous system and activation of
the renin–angiotensin system (p. 625). In contrast, atrial natriuretic peptide
(ANP), produced by the atria of the heart in response to an increase in blood
volume, increases sodium excretion.
Abnormalities of extracellular volume
Increased extracellular volume
Extracellular volume expansion is the result of increased sodium (and hence
water) reabsorption or impaired excretion by the kidney.
Clinical features
These depend on the distribution of excess fluid within the extracellular
space (i.e. between the interstitial space and intravascular compartment),
which in turn depends on venous tone (which determines hydrostatic pressure), capillary permeability, oncotic pressure (mainly dependent on serum
albumin) and lymphatic drainage. As an example, cardiac failure leads to
expansion of both compartments:
• Interstitial volume overload: ankle oedema, pulmonary oedema, pleural
effusion and ascites
• Intravascular volume overload: raised JVP, cardiomegaly and a raised
arterial pressure in some cases.
It is important to differentiate this from local causes of oedema (e.g. ankle
oedema as a result of venous damage following thrombosis), which do not
reflect a disturbance in the control of extracellular volume.
Aetiology
Most causes of extracellular volume expansion are associated with renal
sodium chloride retention.
326 Water, electrolytes and acid–base balance
• Cardiac failure results in a reduction in cardiac output and impaired
perfusion (therefore effective hypovolaemia) of the volume receptors. The
increased sympathetic activity generated by stimulation of the volume
receptors leads to release of antidiuretic hormone (ADH, vasopressin)
even though plasma osmolality (see later) is unchanged.
• Cirrhosis is complex, but there is vasodilatation and underperfusion of
the volume receptors. Hypoalbuminaemia may also contribute.
• Nephrotic syndrome is associated with sodium retention primarily
due to increased sodium reabsorption in the renal collecting tubules
directly induced by the renal disease. In addition, in some patients the
low plasma oncotic pressure induced by hypoalbuminaemia leads to
plasma volume depletion and arterial underfilling as in cardiac failure
and cirrhosis.
• Sodium retention may occur as a result of renal impairment, where
there is a reduction in renal capacity to excrete sodium, or due to drugs
such as mineralocorticoids (aldosterone-like actions), thiazolidinediones
(upregulation of the epithelial sodium transporter channel) and nonsteroidal anti-inflammatory drugs (NSAIDs). The latter inhibit synthesis
of vasodilatory prostaglandins in the kidney with an increase in renal
vascular resistance and an increase in sodium and water reabsorption.
Management
The underlying cause must be treated. The cornerstone of management is
diuretics, which increase sodium and water excretion in the kidney. There are
a number of different classes of diuretic (Table 8.4 and p. 343).
Decreased extracellular volume
Aetiology
Volume depletion occurs in haemorrhage, plasma loss in burns, or loss of
salt and water from the kidneys, gastrointestinal tract or skin (Table 8.5). In
sepsis, signs of volume depletion occur despite a normal or increased body
content of sodium and water due to vasodilatation and increased capillary
permeability.
Clinical features
Symptoms include thirst, nausea and postural dizziness. Interstitial fluid loss
leads to loss of skin turgor while loss of circulating volume causes peripheral
vasoconstriction and tachycardia, a low JVP and postural hypotension. Severe
depletion of circulating volume causes hypotension, which may impair cerebral perfusion, resulting in confusion and eventually coma.
Investigations
The diagnosis is usually made clinically. For patients in critical care, a central
venous line allows measurement of central venous pressure, which will
Regulation of Body Fluid Homeostasis 327
Table 8.4 The main classes of diuretics in clinical use
Class Example Mechanism of action Relative
Loop
diuretics
Thiazides
Aldosterone
antagonists
Potassiumsparing
Furosemide
Bumetanide
Bendroflumethiazide
Hydrochlorothiazide
Spironolactone
Eplerenone
Amiloride Prevent potassium exchange
Reduce Na+ and Cl−
reabsorption in ascending
limb of loop of Henle
Reduce sodium reabsorption
in distal convoluted tubule
Aldosterone antagonist
for sodium in distal tubule
potency
++++
++
+
+
Table 8.5 Causes of extracellular volume depletion
Haemorrhage
External
Concealed, e.g. leaking aortic aneurysm
Burns
Gastrointestinal losses
Vomiting
Diarrhoea
Ileostomy losses
Ileus
Renal losses
Diuretic use
Impaired tubular sodium conservation
Reflux nephropathy
Papillary necrosis
Analgesic nephropathy
Diabetes mellitus
Sickle cell disease
help in assessing the response to treatment. Plasma urea may be raised
because of increased urea reabsorption and, later, prerenal failure (when the
creatinine rises as well). Urinary sodium is low (<20 mmol/L) if the kidneys
are working normally. However, the urinary sodium can be misleading if the
cause of the volume depletion involves the kidneys, e.g. with diuretics or
intrinsic renal disease.
328 Water, electrolytes and acid–base balance
Management
The aim of treatment is to replace what has been lost.
• Haemorrhage involves the loss of whole blood. Immediate treatment is
with crystalloid or colloid until packed red cells are available.
• Loss of plasma (e.g. burns, peritonitis), should be treated with human
plasma or a colloid (p. 324).
• Loss of sodium and water, (e.g. vomiting, diarrhoea or excessive renal
losses) is treated with replacement of water and electrolytes. In chronic
conditions associated with mild/moderate sodium depletion, e.g. saltlosing bowel or renal disease, oral supplements of sodium chloride or
sodium bicarbonate (depending on acid–base balance) may be sufficient.
Glucose–electrolyte solutions are used to restore fluid balance in patients
with diarrhoeal diseases. This is based on the fact that the presence of
glucose stimulates intestinal absorption of salt and water.
• In the acute scenario when there has been significant loss of sodium
and water, patients are usually treated with intravenous sodium chloride
0.9% (see Table 8.3), and replacement is assessed clinically and by
measurement of serum electrolytes.
• Loss of water alone, e.g. diabetes insipidus, only causes extracellular
volume depletion in severe cases because the loss is spread evenly over
all the compartments of body water. The correct treatment is to give
water. If intravenous treatment is required, water is given as glucose 5%
(pure water would cause osmotic lysis of blood cells).
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
Water moves freely between compartments and the distribution is determined
by the osmotic equilibrium between them. The plasma osmolality can be calculated from the plasma concentrations of sodium, urea and glucose, as follows:
Calculated plasma osmolality (mmol) (2 plasma Na )
The factor of 2 applied to sodium concentration allows for associated
anions (chloride and bicarbonate). The other extracellular solutes, e.g.
calcium, potassium and magnesium, and their associated anions exist in
very low concentrations and contribute so little to osmolality that they can
be ignored when calculating the osmolality. The normal plasma osmolality is
285–300 mosmol/kg.
The calculated osmolality is the same as the osmolality measured by
the laboratory, unless there is an unmeasured, osmotically active substance
present (e.g. ethanol, ethylene glycol).
×
[=+
uurea] [glucose]+
+
Plasma Osmolality and Disorders of Sodium Regulation 329
Regulation of body water content
Body water is controlled mainly by changes in the plasma osmolality. An
increased plasma osmolality, sensed by osmoreceptors in the hypothalamus,
causes thirst and the release of ADH from the posterior pituitary, which
increases water reabsorption from the renal collecting ducts. In addition,
non-osmotic stimuli may cause the release of ADH even if serum osmolality is
normal or low. These include hypovolaemia (irrespective of plasma osmolality),
stress (surgery and trauma) and nausea. In contrast, at a plasma osmolality
of less than 275 mosmol/kg there is complete suppression of ADH secretion.
Sodium content is regulated by volume receptors, with water content
adjusted to maintain a normal osmolality and a normal plasma sodium
concentration. Disturbances of sodium concentration are usually caused by
disturbances of water balance, rather than an increase or decrease in total
body sodium.
Hyponatraemia
Hyponatraemia reflects too much water in relation to sodium; affected
patients may or may not have a concurrent abnormality in sodium balance.
Hyponatraemia (serum sodium <135 mmol/L) may be the result of the
following:
• Relative water excess (dilutional hyponatraemia).
• Salt loss in excess of water, e.g. diarrhoea and renal diseases.
• Rarely, pseudohyponatraemia, in which hyperlipidaemia or
hyperproteinaemia results in a spuriously low measured sodium
concentration. The sodium is confined to the aqueous phase but its
concentration is expressed in terms of the total volume of plasma (i.e.
water + lipid). In this situation, plasma osmolality is normal and therefore
treatment of ‘hyponatraemia’ is unnecessary.
• Artefactual ‘hyponatraemia’ caused by taking blood from the drip arm
into which a fluid of low sodium, e.g. 5% glucose, is being infused.
The next step is to assess whether patients are hypovolaemic, euvolaemic
or hypervolaemic (Fig. 8.2). Simultaneous urine and plasma osmolality and
sodium should be measured.
Hyponatraemia resulting from salt loss (hypovolaemic hyponatraemia)
These patients have a deficit of both total body sodium and water, with the
sodium deficit exceeding that of the water. As fluid is lost and the patient
becomes hypovolaemic there is stimulation of volume receptors leading to
thirst and non-osmotic release of ADH. Measurement of urinary sodium helps
differentiate between renal and extrarenal sources of fluid loss (see Fig. 8.2).
For example, vomiting and diarrhoea are associated with avid sodium retention as the kidney responds to volume contraction by conserving sodium
330 Water, electrolytes and acid–base balance
Assess volume status
Hypovolaemia
(hypotensive, postural
drop in BP)
Measure urine sodium
concentration?
>20 mmol/L
Renal losses
Osmotic diuresis
hyperglycaemia
severe uraemia
Diuretics
Adrenocortical
insufficiency
Tubulointerstitial renal
disease
Unilateral renal artery
stenosis
Recovery phase of ATN
Normovolaemia
Severe hypokalaemia
Psychiatric illness
Osmotic ADH release
<20 mmol/L
Extrarenal losses
Vomiting
Diarrhoea
Haemorrhage
Burns
Pancreatitis
Hypothyroidism
SIADH
Hypervolaemia
Heart failure
Liver failure
Oliguric renal failure
Hypoalbuminaemia
Fig. 8.2 Diagnosis of hyponatraemia. Osmotic antidiuretic hormone (ADH)
release refers to unmeasured osmotically active substances stimulating osmotic
release of ADH. These include glucose, mannitol, chronic alcohol abuse and sickcell syndrome (leakage of intracellular ions). SIADH, syndrome of inappropriate
ADH secretion; ATN, acute tubular necrosis; BP, blood pressure.
chloride. Diuretics are the most common cause of hypovolaemic hyponatraemia with a high urinary sodium concentration.
Clinical features
These are usually a result of the hypovolaemia and extracellular volume
depletion (p. 327). Symptoms directly related to the hyponatraemia are rare,
as the loss of both sodium and water limits osmotic shifts in the brain.
Management
Restoration of extracellular volume with crystalloids or colloids interrupts
non-osmotic release of ADH and normalizes serum sodium.
Hyponatraemia resulting from water excess (dilutional hyponatraemia)
An excess of body water relative to sodium is differentiated from hyponatraemia caused by sodium loss because there are none of the clinical features
Plasma Osmolality and Disorders of Sodium Regulation 331
of extracellular volume depletion. This is the most common mechanism of
hyponatraemia seen in hospitalized patients. The most common iatrogenic
cause is overgenerous infusion of 5% glucose in post-operative patients; in
this situation the hyponatraemia is exacerbated by an increased ADH secretion in response to stress.
Aetiology
Hyponatraemia is often seen in patients with severe cardiac failure, cirrhosis
or nephrotic syndrome, in which there is an inability of the kidney to excrete
‘free water’. This is compounded by the use of diuretics. There is evidence
of volume overload and the patient is usually oedematous. Where there is no
evidence of extracellular volume overload (i.e. euvolaemic patient), causes
include the syndrome of inappropriate ADH secretion (SIADH) (p. 630),
Addison’s disease and hypothyroidism.
Clinical features
Symptoms rarely occur until the serum sodium is less than 120 mmol/L and
are more conspicuous when hyponatraemia has developed rapidly, i.e. over
hours. The symptoms result from the movement of water into brain cells
(cerebral oedema) in response to the fall in extracellular osmolality, and
include headache, confusion, convulsions and coma. If hyponatraemia has
developed slowly the brain will adapt by decreasing intracellular osmolality,
and symptoms occur at a lower serum sodium concentration, e.g. <110
mmol/L.
Investigations
Hyponatraemia in association with cardiac failure, cirrhosis or nephrotic
syndrome is usually clinically obvious and no further investigation is necessary. If there is no evidence of volume overload the most probable cause
is SIADH or diuretic therapy. Serum magnesium and potassium must be
checked, as low levels potentiate ADH release and cause diuretic-associated
hyponatraemia.
Management
The underlying cause must be corrected where possible. Most cases (those
without severe symptoms) are simply managed by water restriction (to
1000 mL/day or even 500 mL/day) with a review of diuretic treatment and
other medications associated with hyponatraemia. Management of SIADH is
described on page 631. Patients with hyponatraemia developing acutely are
at the greatest risk of developing cerebral oedema and should be treated
more urgently (Emergency Box 8.1). Administration of desmopressin helps
to avoid acute diuresis.
A vasopressin V2 receptor antagonist, e.g. tolvaptan, which produces
free water diuresis, may be used only under specialist supervision to treat
hyponatraemia.
332 Water, electrolytes and acid–base balance
Emergency Box 8.1 Management of hyponatraemia
resulting from water excess
• Treat the underlying cause.
• Restrict water intake to 500–1000 mL/day and review diuretic therapy.
• Correct magnesium and potassium deficiency.
• Acute symptomatic hyponatraemia and severe neurological impairment
should be managed in a critical care setting:
• Infuse hypertonic saline, e.g. 3% saline (513 mmol/L) at a rate of 1–2
mL/kg/h; 1 mL/kg will raise plasma sodium by 1 mmol/L assuming
that total body water comprises 50% of total body weight.
• Aim to raise serum sodium by 8–10 mmol/L in the first 24 hours and
8 mmol/L in each 24-hour period thereafter.
• Give furosemide 40–80 mg i.v. to enhance free water excretion.
• Serum sodium should not be corrected to greater than 125–130 mmol/L.
• Hypertonic saline is contraindicated in patients who are fluid
overloaded; give 100 mL of 20% mannitol.
Central pontine myelinolysis
Over-rapid correction of the sodium concentration must be avoided, as this
can result in a severe, neurological syndrome due to local areas of demyelination, called central pontine myelinolysis or the osmotic demyelination
syndrome. Features of this include quadriparesis, respiratory arrest, pseudobulbar palsy, mutism and, rarely, seizures. The distribution of the areas
of demyelination include most often the pons, but also, in some cases, the
basal ganglia, internal capsule, lateral geniculate body and even the cerebral cortex. Diagnosis is by characteristic appearances on brain magnetic
resonance imaging (MRI).
Hypernatraemia
Hypernatraemia (serum sodium >145 mmol/L) is almost always the result of
reduced water intake or water loss in excess of sodium. Less commonly, it is
due to excessive administration of sodium, e.g. as intravenous fluids (sodium
bicarbonate or sodium chloride 0.9%) or administration of drugs with a high
sodium content.
Aetiology
Insufficient fluid intake is most often found in elderly people, neonates or
unconscious patients when access to water is denied or confusion or coma
eliminates the normal response to thirst. The situation is exacerbated by
increased loss of fluid, e.g. sweating, diarrhoea.