Sodium disorders in neuroanaesthesia and neurocritical care Flashcards
Normal Sodium Homeostasis
- Concentration normally maintained 135-145mmol/L
- Main contributor to serum osmolality 280-295mOsm/kg
Brain Control
- Increased serum osmolality causes the hypothalamic osmoreceptors to stimulate ADH secretion from the posterior pituitary
- RAAS activation stimulates thirst and increased water consumption
Renal Control
- Total body sodium is regulated by renal excretion
- Reabsorption is controlled by the sympathetic system, ANP and BNP
Cardiovascular Control
- Reduction in plasma volume stimulates the carotid baroreceptors and the rt atrial baroreceptors
- This stimulates RAAS activation
Causes of hyponatraemia
Hypovolaemic
- Cerebral salt wasting syndrome
- Hypokalemia
- Diuretics
- Primary adrenal insufficiency
- Ketonuria
- Diarrhoea and vomiting
- Blood loss
Euvolaemic
- SIADH
- Hypothyroidism
- Secondary adrenal insufficiency
- Brain metastases
Hypervolaemic
- SIADH
- Congestive heart failure
- Cirrhosis
- Renal failure
- Anaphylaxis
- Pregnancy
Causes of hypernatraemia in neurointensive care
Diabetes insipidus
- Following pituitary surgery
- SAH
- Traumatic brain injury
Iatrogenic
- Use of mannitol or 8.4% NaHCO3
Clinical features of hyponatraemia
- Lethargy
- N&V
- Anorexia
- Headache
- Muscle weakness
- Seizures and confusion
- Coma
Clinical features of hypernatraemia
- Thirst
- Lethargy
- Muscle weakness
- Confusion
- Coma
Pathophysiology of SIADH
- Inappropriate ADH secretion leading to increased water reabsorption
- Causes a dilutional hyponatraemia in a clinically euvolemic patient
- Causes: SAH, intracerebral and subdural haematoma, brain tumours, meningitis, encephalitis and traumatic brain injury
Pathophysiology of cerebral salt wasting syndrome
- Damaged sympathetic system failing to support sodium reabsorption because of hypothalamic damage
- Increased ANP and BNP release centrally after injury leading to increased sodium and water excretion
- Causes: SAH, traumatic brain injury, stroke, TB meningitis
How quickly should sodium be corrected
- Max of 10mmol/L in 24 hrs
- Risk of central pontine demyelination (osmotic demyelination syndrome) causing quadriplegia, dysphagia, dysarthria and locked-in syndrome
Treatment of SIADH vs Cerebral Salt Wasting Syndrome
SIADH
- Fluid restrict
- If symptomatic or unable to restrict then given hypertonic saline with careful Na monitoring
Cerebral Salt Wasting Syndrome
- Resuscitate with 0.9% NaCl
- Hypertonic saline may be required
- Fludrocortisone can be used for refractory cases and salt tablets
Pathophysiology of central diabetes insipidus
- Damage to the hypothalamic-pituitary axis leading to no ADH being released
- Often after pituitary surgery or craniopharyngioma surgery or brain stem death
- No water reabsorption occurs and Na is lost as it is pulled out as a solute
- Leads to hypernatraemia and dehydration
Diagnosis of diabetes insipidus
- High urine output (>1L in 4 hours)
- Hypernatraemia
- urine specific gravity <1.005
Emergency management of severe hyponatraemia (<125mmol/L) or seizures as a result of hyponatraemia
- 150ml of 3% NaCl (ideally through a CVC) over 20 mins
- Check U&Es
- Repeat bolus until a rise of 5mmol/L occurs in one dour
- If not responding start an infusion of hypertonic saline aiming for a rise of 1mmol/L per hour
- No more than 10mmol/L in 24 hours.
- Catheter and urine output monitoring
Treatment algorithm for severe (>155) Hypernatraemia
Treat for central diabetes insipidus if…
- CVP<5
- Urine output >1000ml in 4 hours
- Specific gravity <1.005
- Normal urinary sodium and low urine osmolality
- High serum osmolality and sodium
Treatment: 0.2-0.4mcg IV bolus of DDAVP, consider 5% dextrose IV infusion if feasible safer to use NG or oral water. Do not reduce sodium by >10mmol/24 hours
Treat for dehydration if…
- CVP <5
- Low urine output <0.5ml/kg/hr
- High specific gravity >1.02
- Tachycardia and hypotension
Treatment: IV fluid resuscitation with isotonic fluids. Do not reduce sodium by >10mmol/24 hours
