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4 Chapter 1: Principles and practice of medicine and surgery
release stimulating water reabsorption by the kidneys. Management
Watermoving out of cells causes the cells to shrink. The aim is to gradually reduce the serum sodium con-
In response to this, electrolytes are transported across centration by no more than 0.5–1 mmol/L/h in order
the cell membrane, changing the membrane potential. to avoid cerebral oedema. Urine output and plasma
Changes in the membrane potential in the brain leads to sodium should be monitored frequently. The under-
impaired neuronal function and if there is severe shrink- lying cause should also be looked for and treated.
age, bridging veins are stretched leading to intracranial If the patient is alert and conscious he/she should be
haemorrhage.Cellsalsobegintoproduceorganicsolutes allowedtodrinkfreelyasthisisthesafestwaytocorrect
after about 24 hours to draw fluid back into the cell. hypernatraemia.
If the patient is fluid depleted, intravenous replace-
ment should be with 0.9% saline to restore intravascu-
Clinical features
lar volume. In severe hypernatraemia even 0.9% saline
The symptoms of hypernatraemia include thirst, nausea
is less hypertonic than the plasma so this will help to
and vomiting. Patients may be irritable or tired, pro-
correct the high sodium.
gressing to confusion and finally coma. On examination
If the patient is not fluid depleted but is unable to
there may be features of fluid depletion including re-
drink, 5% dextrose is given slowly.
duced skin turgor, hypotension, tachycardia, peripheral
In hyperosmolar non-ketotic coma saline or half-
shutdown and reduced urine output. Signs of fluid over-
normal saline (0.45% saline) should be used until glu-
load suggest excessive administration of salt or Conn’s
coseconcentrationsarenearnormal.Thisistoprevent
syndrome. Polyuria and polydipsia suggest diabetes in-
worsening hyperglycaemia which can alter the osmo-
sipidus or hyperglycaemia. There may be neurological
lality further.
signs such as tremor, hyperreflexia or seizures.
Prognosis
Complications
The mortality rate of severe hypernatraemia is as high as
Hypernatraemicencephalopathyandintracranialhaem-
60% often due to coexistent disease, and there is a high
orrhage (may be cerebral, subdural or subarachnoid)
risk of permanent neurological deficit.
may occur in severe cases. Too rapid rehydration can
cause cerebral oedema as the cells cannot clear the or-
ganic solutes rapidly.
Hyponatraemia
Definition
Investigations
Aserum sodium concentration <135 mmol/L.
The diagnosis is confirmed by the finding of high
serum sodium on U&Es. Serum glucose and urine
sodium, potassium and osmolality should also be re- Incidence
quested. If there is raised urine osmolality, this is a sign Occurs relatively commonly, with 1% of hospitalised pa-
that the kidneys are responding normally to hyperna- tients affected.
traemia by producing low volume, high concentration
urine. The underlying cause is therefore due to non-
Age
renal fluid losses.
Any. Young and old are at greater risk.
Conn’s syndrome or ectopic ACTH syndrome is sug-
gested by a mild hypernatraemia, hypertension, hy-
Sex
pokalaemia (in the absence of diuretic drugs used to
M = F
treat hypertension) and a raised urinary potassium.
CT scan of the head is indicated if there are neurolog-
ical symptoms or signs, and in severe hypernatraemia Aetiology
to look for an underlying cause (such as head trauma) The causes of hyponatraemia are given in Table 1.1. It is
or complications such as haemorrhage. most useful to consider the causes according to whether