Electrolyte and endocrine disturbances
- Na Disorders
- Common after TBI
- Hypo- and hypernatraemia have adverse effects on the injured brain.
- A systematic approach to diagnosis and treatment is essential.
- ADH, antidiuretic hormone; CDI, central diabetes insipidus; CSWS, cerebral salt wasting syndrome; DDAVP, 1-deamino-8-D-arginine vasopressin; SIADH, syndrome of inappropriate ADH secretion.
Finding | SIADH | CSWS | CDI |
Plasma volume | Raised | Lowered | Lowered |
Sodium balance | Positive/equal | Negative | Equal |
Water balance | Positive | Negative | Negative |
Serum sodium | Low | Low | High |
Serum osmolality | Lowered | High/normal | High |
Urine sodium | High | High | Normal |
Urine osmolality | High | Normal/high | Low |
Management | - Electrolyte-free water restriction—initially to 1000–1500 ml/day—if cardiovascular status allows - Demeclocycline—inhibits renal response to ADH - ADH-receptor antagonists—inhibit binding of ADH to renal receptors | - Volume and sodium resuscitation - Fludrocortisone may limit sodium loss | - Replace fluids to maintain normovolaemia - DDAVP if high urine output (>250 ml/h) continues |
Magnesium for neuro-protection in head injury
- Double blind parallel group randomised trial, Class II evidence
- N = 499, Seattle, 1998-2004
- Primary outcome: functional status, seizures, neuropsychological tests
- Conclusions:
- IV magnesium sulphate given within 8hr of moderate to severe TBI does not improve outcome and may have detrimental effect
- Critique:
- Single centre study
- Composite outcome measure including 39 measures