Hyponatraemia

Clinical Cases

Cause of HYPOnatraemia

  • Definition: Serum sodium <130mEq/l
  • Cause: Excess of Water relative to Sodium
  • Affects: 1% of hospital population
  • Hypovolemic (Na deficit in xs of water deficit) (test urine sodium)
    • RENAL (urinary Na >20mmol)
      • Addison’s
      • Renal failure (Diuretic stage)
      • Salt losing nephropathy (RTA)
      • Diuretic- Thiazides and osmotic diuretics
      • Cerebral salt wasting
    • PRE-RENAL (Urinary Na <20mmol)
      • Third space losses (Burns, pancreatitis, bowel obstruction, cirrhosis)
      • Sweating/vomiting/diarrhoea with continued water intake
        • Alkalosis with upper GI and skin loss
        • Acidosis with lower GI loss
  • Normovolemic (Test urine osmolality)
    • Urine osmolality <serum osmolality
    • Urine osmolality > serum osmolality
      • SIADH (urine Na >20mmol
        • Malignancy (lung, pancreas, prostate, lymphoma, others)
        • CNS, Lung infection and granulomatous disease, Porphyria, positive pressure ventilation
        • Drugs: Psychoactive- MAOI, SSRI, TCA, NSAID, chlorpromazine, Chemotherapeutic (induce SIADH)
  • Hypervolemic (increased TBW relative to Na) (oedematous states)
    • Urinary sodium <20mmol/l
      • Increased interstitial salt
      • Low albumin and secondary hyperaldosteronism
      • CCF, cirrhosis, nephrotic syndrome, hepato-renal syndrome
    • Urinary sodium >20mmol/l
      • Renal failure
      • Hypertonic saline, early diuretics
      • Hypothyroidism
  • Fictitious (Pseudohyponatraemia)
    • Hyperglycaemia (draws water to ECF)
      • Corrected sodium…Measured Na + [glucose - 5]/4
    • Hyperproteinemia, hyperlipidemia
    • Mannitol
    • Glyceine washout for TURP and hysteroscopy

Hyponatraemia Interpretation Flow Diagram

Click to enlarge

Clinical

Severity of symptoms associated with rapidity of loss and extent of fall

  • >125      Asymptomatic
  • 115-125 Lethargy, confusion, anorexia, nausea, vomiting
  • <115      Muscle cramps and weakness, convulsions, coma

Complication

  • Cerebral oedema
    • Secondary to abrupt sodium losses and free water shift from vascular to interstitial space
  • ECG changes
    • Cause of non-ischaemic ST elevation on ECG
  • Pontine demyelinosis (no clear evidence that associated with rapid correction)
    • Develops 3-5 days after treatment
      • Demyelination of central pons, corticobulbar and corticospinal tracts
      • Altered mental state, pseudobulbar palsies
      • Dysphasia and spastic quadriparesis
    • More likely in chronic hyponatraemia

Correction

Depends on rapidity of onset and clinical symptoms

  • Asymptomatic hyponatremia
    • Slow at 0.5mEq/hr (max 12mmol/24 hours)
    • Rapid correction may lead to pontine myelinolysis
      • Water restriction is usually used (especially in SIADH)
      • Salt tablets and diuretics
      • Demeclocycline
    • Induces nephrogenic diabetes insipidus
    • Use with caution, potentially nephrotoxic
  • Symptomatic with neurological symptoms
    • Initial rate 1-2mmol/hr for first few hours
    • Monitor CNS symptoms regularly
    • Revert to 0.5mEq/hr after stable

Calculations:

  • Calculate Na deficit

Na deficit= (desired Na-current Na) x (0.6 x body weight)

Correction

  • In acute severe hyponatraemia, aim for 1-2mEq/hour correction
  • In chronic severe hyponatraemia aim for 0.5-1mEq/hour correction.
  • Hypertonic saline replacement
    • 3% saline (513mEq/L) by giving (deficit/513) to the patient at the rate of 1mEq/hour over 4 hours
  • New AVP receptor antagonists are currently undergoing phase III clinical trials and show promise for the treatment of hyponatraemia.  The increase serum sodium by stimulating free water excretion.
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