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hyponatraemia

hyponatraemia

introduction

  • hyponatremia is a serum sodium < 135 mmol/L
  • most cases are caused by excessive water intake (oral or iv) and subsequent retention of water, particularly at risk are those with impaired ability to suppress ADH secretion, or if they have primary polydipsia which overwhelms the renal ability to excrete water (max. amount normal people can excrete is ~10L/day)
  • some cases are associated with dehydration

clinical effects

  • patients with chronic levels of 120mEq/L or higher are generally asymptomatic although may have subtle neurologic impairments and increased falls risk
  • severe neurologic symptoms are most likely to occur with acute hyponatraemia (occurring in less than 24hrs before cerebral protective processes are in place), and with severe hyponatraemia with levels below 125 mmol/L and are most likely to occur due to acute events such as:
    • severe prolonged exercise
    • primary polydipsia
    • iatrogenic excessive water administration in patients with impaired renal water excretion such as with post-op patients with syndrome of inappropriate ADH secretion (SIADH)
    • MDMA (ecstasy) use
  • neurologic effects include:
    • impaired cognition, dizziness, gait disturbances, memory losses, lethargy
    • cerebral oedema
    • cerebral herniation

aetiology

artefactual

  • drawing blood from an iv site which has had recent iv fluids running
    • actual serum sodium must be corrected to account for high glucose levels
  • pseudohyponatraemia due to high lipid or protein levels

hyponatraemia with low serum osmolality

  • this is usually due to excessive ADH secretion due to either:
    • pathophysiologic drive from baroreceptors detecting low effective arterial BP:
      • true volume depletion:
        • urine sodium will be < 20mM but this may also occur with hypervolaemia
        • extreme exercise with mainly water intake and persistent ADH secretion
        • diuretics:
          • Thiazide diuretics in particular may cause hyponatraemia, esp. soon after starting Rx due to:
          • direct reduction in renal distal tubular NaCl reabsorption with impaired water excretion due to increased ADH actions resulting in urinary sodium + potassium concentrations exceeding plasma concentrations
        • primary adrenal insufficiency (Addisonian crisis) with aldosterone deficiency
      • with hypervolaemia:
        • cardiac failure:
        • cirrhosis:
          • see cirrhosis - levels are usually > 130mE/L unless end stage disease
    • inappropriate ADH secretion:
      • usually euvolaemic with a high urine osmolality and urine sodium > 20mM
      • secondary adrenal insufficiency
        • as aldosterone secretion usually is unaffected, a low BP and muscle spasms do not usually occur in constrat to primary adrenal insufficiency where there is alos low aldosterone levels
        • caused by low ACTH which may be due to either:
          • pituitary pathology
          • prolonged exogenous glucorticoid use
      • pregnancy tends to reset the osmostat so serum sodium tends to be 5 mmol/L lower
      • ectopic atrial natriuretic peptide production in patienst with small cell tumours of lung
      • nausea
      • stress
  • may be due to excessive water intake overwhelming renal water excretion capabilities:
    • maximally dilute urine has an osmolality of < 100 mmol/kg, if it is higher than this in a euvolaemic patient with hyponatraemia then it suggests there is either syndrome of inappropriate ADH secretion (SIADH) or something preventing maximum dilution such as diuretic Rx contributing to the problem
    • primary polydipsia
      • psychogenic
      • MDMA (ecstasy) - also may cause SIADH
      • hypothalamic lesions (eg. sarcoidosis)
    • iatrogenic
  • may be due to inadequate salt intake:
    • eg. drinking excessive water in heat stress with high salt losses from perspiration, etc

hyponatraemia with normal serum osmolality

  • pseudohyponatraemia due to high lipid or protein levels:
    • marked elevations in serum lipids or proteins result in a reduction in the fraction of serum that is water and an artificially low serum sodium concentration
    • usually lipids and proteins account for ~7% of plasma volume, thus actual sodium concentration in the water component is actually higher than measured by the lab (actual = measured / fraction water in plasma)
    • decreasing the fraction water of plasma by having more lipids or proteins will decrease the measured sodium concentration but actual water concentration of sodium will be the same.
  • advanced renal failure:
    • advanced renal failure can impair free water excretion and serum osmolality may be normal or high due to high blood urea levels
    • note that urea is an ineffective osmole as it can freely cross cell membranes and thus effective serum osmolality is often low once the urea component is subtracted from measured levels.
  • low protein diets:
    • normal diets result in 600-900 mosmol of solute (mainly sodium, potassium and urea) excreted renally per day
    • minimum urine osmolarity is ~60mosmol/kg urine
    • thus low protein diets such as tea and toast only, have reduced water excretion capability due to decreased solute excretion
    • beer contains minimal sodium, potassium or protein and suppresses muscle breakdown thus further reducing urea production, resulting in solute excretions of only 250 mosmol/day and maximum urine output of only 4L/day.
  • non-sodium nonconductive irrigation solutions absorbed into ECFV:
    • glycine or sorbitol solutions used in TURP, laparoscopy or hysteroscopy

hyponatraemia with high serum osmolality

  • artefactual in severe hyperglycaemia:
    • for glucose levels up to 22mmol/L, need to apply a correction factor of 1.6mEq/L per 5mmol/L elevation of glucose
    • for glucose levels above 22mmol/L, need to apply a higher rate of correction of 4mEq/L per 5mmol/L elevation of glucose above 22mmol/L
    • these calculations are generally used to predict how much serum sodium will rise once hyperglycaemia is corrected
  • hypertonic Rx:

drug-induced hyponatraemia

  • ADRAC reported events in Australia 2005-20081):
    • 307 reports of which 227 implicate a single drug, mainly diuretics (126)and antidepressants (78 - 33 were a SSRI or SNRI)
    • 80 involved multiple agents, often diuretic combined with ACEI, angiotensin II blocker, or SSRI or SNRI, or carbamazepine.
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hyponatremia
hyponatraemia.txt · Last modified: 2018/08/29 11:41 by wh