- Hyponatraemia after subarachnoid haemorrhage (SAH) has prevalence rates of approximately 30-55%
- The blood/urine osmolality and electrolyte testing might be the same for both conditions
- The aetiology of hyponatraemia after SAH
- SIADH
- Cerebral salt wasting
- Acute ACTH/glucocorticoid deficiency
- Excess iv fluids
- Diuretic therapy
- Fluid restriction is typically not used to normalise serum sodium in critical, symptomatic patients for fear of exacerbating hypovolemia and increasing the risk of cerebral ischaemic.
SIADH vs CSW
- Hyponatremia following mild/moderate subarachnoid hemorrhage is most likely due to SIADH and glucocorticoid deficiency and not cerebral salt wasting
- Hyponatremia due to SIADH is transient after SAH
- Relationship between plasma AVP concentrations and plasma osmolality was lost in patients with SIADH
- 0900 hour plasma cortisol concentrations <300 nmol/L represented inappropriate hypocortisolemia after SAH
- Most patients who developed acute hypocortisolemia did not develop hyponatremia, so hyponatremia was not a sensitive marker for the identification of acute ACTH deficiency.
- True cerebral salt wasting is very rare and even a consultant endocrinologist probably sees less than 5 in his whole career
- Slow correction to avoid osmotic demyelination syndrome (eg central pontine myelinolysis)
- Correct < 0.5 mEq/L/hr
- S&S of demyelination (initially S&S improve as Na increases then deteriorates with the following)
- Flaccid/spastic quadriplegia
- Mental status changes
- Cranial nerve abnormalities: pseudobulbar palsy
- Neurological effects mimic spasm
- 3x more likely to have infarction than normonatremic patients
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