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Any intracranial disease, surgery, mechanical ventilation,
and anesthetics may be complicated with electrolyte imbalance. They are
more common in SAH & head injuries. Both pathophysiological processes
and therapeutic maneuvers may lead to a number of abnormalities in fluid
and electrolytes. They are attributed to lesions of the hypothalamus.
The incidence is about 10% of which hyponatremia is the most
common with a mortality rate of about 15% whereas hypernatremia has the
highest mortality rate (42%).
HYPONATREMIA:
Hyponatremia (Serum Sodium level less than 135 mEq/L) has
usually been associated with SIHADH, but recent reports suggest that
hyponatremia can be caused by natriuresis due to the so called 'Cerebral
Salt Wasting' (True sodium Depletion). There may not be decrease in the total exchangable body
sodium and may just be a shift into the third space or into the cells
leading to decrease in sodium in ECF. Both
syndromes are characterized by a decrease in serum sodium levels and
osmolality.
Clinical features include nausea, vomiting, irritability,
personality changes anorexia convulsions and coma, in fact the features
may simulate features of coning.
Cerebral salt wasting:
In this syndrome, hyposmolality is caused by primary loss of
sodium in the urine, resulting in serum hypotonicity which in turn
inhibits thirst and secretion of ADH which results in hypovolemic
hyponatremia with clinical and
investigative picture of dehydration.. In
the absence of adrenal insufficiency, renal disease or diuretic use which
may display a similar picture, this syndrome is attributed to an
unidentified natriuretic factor in the brain, probably in the region of
the roof of the IV ventricle.
Clinically there is low or postural hypotension, with
tachycardia and other signs of dehydration in addition to the cerebral
symptoms of hyponatremia.
SIHADH:
This refers to increased release of ADH that is
inappropriate to the serum osmolality. Clinical features include normal
skin turgor and blood pressure with absence of peripheral edema with
serum hyponatremia & hypo-osmolality. This is characterised by
hyponatraemia, hypo-osmolality, urine osmolality greater than serum
osmolality, continued loss of sodium inspite of hyponatraemia; in absence
of renal function disorders and endocrine dysfuction. In normal
circumstances, the osmolality is maintained by absorption of sodium by
renal tubules. In SIADH there is suppression of aldesterone secretion
resulting in disproportionate loss of sodium in urine further depleting
sodium store in ECF. In a chronic stage, the extracellular water egresses
into the cellular compartment reducing circulating volume and producing
shock. This state of shock does not respond to pressure agents and need
fluid replacement. Cerebral abscess, hypopituitarism, encephalitis,
Gullain Barre Syndrome, head injuries, meningitis, subarachnoid
haemorrhage, concussion, electroconvulsive therapy and many other stress
reactions precipitate SIADH. Drugs like hypoglycaemic agent,
antineoplastic agents, tricylcic antidepressants, diuretics can
precipitate SIADH.
Other causes:
Hyponatremia may be caused by the presence of other
osmotically active substances in the blood, common examples being
mannitol and glucose. In these instances, since plasma tonicity is normal
or even elevated, hyponatremia does not promote cerebral symptoms.
Management:
Patients remain asymptomatic with sodium levels above
125mEq/L and may be observed with unrestricted salt intake. Serious
neurological problems appear when the level goes below 115mEq/L and
require intensive management. Cerebral salt wasting requires fluid
replacement whereas SIHADH requires fluid restriction. Hence it is
essential to diagnose the cause of hyponatremia.
More often than not clinical examination and basic
investigations may not help.
The following guidelines will help
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PARAMETER
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SIHADH
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CEREBAL
SALT WASTING
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Blood Pressure
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Normal
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Low or Normal
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Heart Rate
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Slow or Normal
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Tachycardia or normal
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Hematocrit
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Normal or Slow
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Elevated
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GFR
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Increased
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Decreased
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Urea or Creatinine
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Normal or Low
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Normal or High
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Urine Volume
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Normal or Low
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Normal or High
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Urine Concentration
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High
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High
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Blood Volume
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Increased or Normal
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Decreased
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Hydration
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Well hydrated
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Decreased
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Body Weight
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Normal or Increased
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Decreased
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Average Day of Appearance
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8th Day
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4-5th Day
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Recent reports suggest SIHADH is more common in lesions
around hypothalamus and salt wasting is more common when there is
generalized brain involvement (SAH and head injuries).
As one will appreciate from the above parameters the most
reliable test to differentiate between SIHADH & Salt wasting is to
measure the Serum ADH which is not possible. Blood volume measurement is
not practicable in Indian setting. CVP measurements will help to assess
blood volume & is a must in the management. Higher urinary specific
gravity/spot sodium may suggest salt wasting.
In cerebral salt wasting volume replacement with normal
saline should be instituted.
Before starting the treatment for hyponatraemia, true
hyponatraemia should be established. The following steps are suggested :
1.
Rule out lab error- Repeat the investigation.
- Calculate Anion gap: {(S. Sodium+S Potassium+ S. calcium)-(S. Bicarbonate +S. Chloride)} which is normally 12 to 16 mEq/L. Any value less than
9mEq/L would most likely be due to lab error.
2.Hyperlipidaemia
3.Hyperproteinaemia
4.Hyperglycaemia ( every increase of glucose by 100mg/dl
would decrease serum
sodium by 1.6mE/L)
Mild to moderate hyponatremia due to SIHADH responds to
fluid restriction in the region of 600-800ml/day. This may not be
feasible in the critically ill who may require minimum fluid load greater
than this, simply to administer medication and to maintain cerebral
perfusion pressure.
A few methods of calculations have been suggested to decide
on the volume of fluid and sodium to be used :
1.
According to weight loss ( assuming that normal S. Sodium is 142mE/L)
Loss
of sodium in mE/L = 142´loss
of weight in Kg
1 mE sodium
= 1 ml hypertonic 5% sodium chloride solution
= 6
ml of isotonic 0.9% sodium chloride solution
2.According to haematocrit level (assuming only
extracellular water and electrolytes
have been lost and there was no hemorrhage)
Normal ECF =
(20% of body weight of which 20% is plasma ) 14 liters
Average
hematocrit = 42% ±in
female , 47% ± in
males
e.g. if
hematocrit is 55% i.e. (55-42=13) 13% more concentrated,
hematocrit loss is 13/42=25%
25% of 14
liters = 3.5%
So, 3.5 L
of isotonic normal saline is urgently needed.
2.
Change of concentration of Sodium
Total
body water volume = 60% of weight = 42 liters in a 70Kg person
Unit Sodium deficit in mE/L = (142 mE/L-
patient’s level of sodium)
Only 50% of
this needs to be corrected
Alternate treatment consists of demeclocycline (600-1200mg/day)
which inhibits the action of ADH on kidney, sodium phenytoin, which
reduces the secretion of ADH from pituitary and lithium carbonate.
Marked hyponatremia may require hypertonic saline (3%- 5%)
infusion (250ml -1500ml) over 6-8 hours in addition to decreasing free
water with frusemide in doses up to 1mgm/kg.
The sodium should never be corrected rapidly, more than 0.5
mEq/L per hour. Correction with hypertonic solution should be
discontinued after the sodium level reaches 125 mEq/L.
Investigation and treatment of the underlying disease should
be carried out along with the management of hyponatraemia including
discontinuation of the attributing drugs.
Monitoring of other electrolytes like potassium and their
simultaneous management is equally important during the management of hyponatraemia.
HYPERNATREMIA:
Hypernatremia and hyperosmolality commonly result from fluid
restriction, osmotic challenge ( Mannitol & tube feeding ) and
diabetes insipidus which is a result of failure of ADH release despite an
adequate osmotic stimulus. The diagnosis of iatrogenic cause should be
apparent by review of the intake and output and drug charts. These
resolve with appropriate fluid replacement.
Diabetes insipidus can be defined as an hourly urine output
of greater than 300ml with urinary specific gravity of less than 1.003
persisting more than 2 consecutive hrs. Awake patients may regulate their
own intake whereas in the obtunded patients, losses from urine output can
be replaced intravenously. Prolonged chasing can result in nephrogenic
diabetes insipidus that is unresponsive to subsequent ADH.
With frank D.I, 5-10 units aqueous pitressin I.V. or I.M.
which may be repeated after 6-8 hours. When permanent D.I develops, therapy
is started with pitressin tannate in oil which has prolonged action
(12-36hrs). Long term therapy is conveniently continued with desmopressin
acetate by nasal insufflations.
To sum up, in cases neurological deterioration with no
obvious surgical cause , electrolyte disturbances should be suspected in
addition to hypoxia and hypercapnia. With its high morbidity and
morbidity electrolyte imbalance warrants prompt detection and appropriate
treatment.
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