Sodium in Neurosurgery:


Dr. A. Vincent Thamburaj,   

Neurosurgeon, Apollo Hospitals,  Chennai , India.

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 (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.


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.


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




Blood Pressure


Low or Normal

Heart Rate

Slow or Normal

Tachycardia or normal


Normal or Slow





Urea or Creatinine

Normal or Low

Normal or High

Urine Volume

Normal or Low

Normal or High

Urine Concentration



Blood Volume

Increased or Normal



Well hydrated


Body Weight

Normal or Increased


Average Day of Appearance

8th Day

4-5th Day

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.



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 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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