FRCA Notes

Sodium Disorders in Head Injured Patients

The curriculum asks for knowledge of 'fluid and electrolyte balance in the head injured patient'.

Differentiating between cerebral salt wasting and SIADH appeared as part of a CRQ on hyponatraemia in 2024.

Resources

  • Sodium disorders after TBI can cause either:
    • Hypontraemia - due to cerebral salt wasting syndrome or SIADH
    • Hypernatraemia - due to diabetes insipidus
  • SIADH
  • CSW
  • Central DI
  • Mannitol-induced diuresis
  • Use of hypertonic saline
  • Dehydration with poor oral intake because of reduced GCS
  • Volume overload e.g. transfusion, crystalloid in resuscitation
  • Diuresis due to other physiological derangement e.g. hypertension, hypothermia, hyperglycaemia
  • Post-obstructive diuresis following urinary retention
  • Effects of drugs e.g. stress ulcer prophylaxis with PPIs, various anti-epileptic drugs

  • Unregulated ADH secretion in the absence of an osmotic trigger e.g. due to brain injury
  • There is an inappropriately high level of ADH
  • There is also a lack of feedback response, such that water is indiscriminately reabsorbed

Characteristics

  • Hyponatraemia (<135mmol/L)
  • Reduced serum osmolality (<280mOsm/kg)
  • Urine osmolality greater than serum osmolality
  • Low urine output (the best way to differentiate between SIADH and CSW)
  • Normovolaemia / hypervolaemia

Management

  • Treat underlying cause
  • Fluid restriction
  • Furosemide: encourages water excretion
  • Demeclocycline: inhibits renal ADH response / direct ADH receptor antagonist

  • A poorly-understood renal loss of sodium during intracranial disorders, in the presence of normal renal function
  • There is increased glomerular filtration due to:
    • Increased release of natriuretic peptides (ANP and BNP)
    • Increased sympathetic activity
  • This leads to natriuresis, and thus polyuria & hypovolaemia
  • There is also a high level of serum ADH, but this is an appropriate response to hypovolaemia

Characteristics

  • Hyponatraemia, although normal sodium is possible
  • Reduced serum osmolality, although normal osmolality is possible
  • High urine osmolality (because of sodium in urine)
  • High urinary sodium
  • High urine output (because water follows salt)
  • Hypovolaemia due to loss of salt and water

Management

  • Replacement of salt and water e.g. with normal saline
  • If normal saline fails, subsequent management involves:
    • Hypertonic saline
    • Fludrocortisone

  • Arises due to either or both of:
    • A failure of ADH secretion e.g. due to posterior pituitary gland damage
    • Reduced activity of ADH on the renal collecting duct

  • Without ADH there is no re-absorption of water at the collecting duct, but there is renal conservation of sodium
  • There is loss of plasma as urine, leading to:
    • Hypovolaemia (leading to hypotension and impaired CPP)
    • Hypernatraemia (associated with increased mortality)
    • Normal urinary sodium concentration

Classification & aetiology

Central DI Nephrogenic DI
Traumatic brain injury (20-35%) Hereditary
ICH Lithium treatment
SAH Hypercalcaemia
Pituitary surgery Hypokalaemia
End-stage cerebral oedema Alcohol intoxication

Risk factors in TBI

  • Severe TBI
  • Base of skull fracture
  • Cerebral oedema on CT
  • Hypothalamic oedema

Diagnostic criteria

  • An increased urine output
    • >1,000ml/4hrs (>250ml/hr)
    • >3,000ml/24hrs

  • High serum sodium >145mmol/L
  • High serum osmolarity >305mosm/kg
  • Low urine osmolarity <350mosm/kg
  • Low urine specific gravity <1.01

Management

  • Generally reserved for when the sodium is >150-155mmol/L
  • Replace the lost fluid e.g. 0.9% NaCl
  • DDAVP (desmopressin) 0.5µg IV PRN