Hyponatreamia

Hyponatraemia John Foote Causes, assessment and management

Hyponatraemia Definitions Significance Pathophysiology Investigation and assessment Management

Acute Hyponatreamia Hyponatraemia which has developed in less than 12-24 hours Leads to water migration from ECF to ICF Clinical issue is with cerebral swelling Symptomatic at < 125 mmol/l

Acute Hyponatraemia and Cerebral Swelling Hyponatreamia Normal

Symptoms of Acute Hyponatraemia Nausea/vomiting Headache Muscular twitching Cognitive impairment Psychosis Convulsions Coma

Chronic Hyponatraemia Hyponatreamia which has developed over more than 24 hours ICF solute discarded to match reduced ECF sodium loss Water distribution between ICF and ECF is undisturbed

Chronic Hyponatraemia Symptoms develop due to neuronal electrolyte depletion with serum [Na + ] at about 115 mmol/l Rapid correction of hyponatraemia leads to brain shrinkage and risk of central pontine myelinolysis

Central Pontine Myelinolysis Onset occurs 24-48 hours after the over-rapid correction of hyponatraemia Devastating neurological deficit Quadraparesis Psuedobulbar palsy Mutism Convulsions Malnourished or alcohol dependent patients at very high risk

Water Homeostasis Plasma Osmolality (mOsmol/Kg) Oral water intake Renal water clearance 270 280 290 300

Osmolar Control of ADH Secretion 270 280 290 300 Plasma Osmolality (mOsmol/Kg) Plasma ADH

Non-osmolar Stimulation of ADH Secretion Hypovolaemia Systemic hypotension Trauma Highly potent mechanism Non-osmolar stimuli are implicated in 95% of cases of severe hyponatraemia

Response to Vascular Volume Deficit Vascular volume deficit Osmolar ADH control Non-osmolar ADH control Vascular volume maintained at the cost of ECF dilution Volume deficit

Investigation Pitfall Urine : serum osmolality measurements which are ‘inappropriately raised’ are non-specific, are often over-reported on laboratory reports, and can be misleading

Diagnosis and Assessment Serum sodium concentrations reflect the ratio between water and sodium content of ECF rather than the absolute amount of either In clinical practice hyponatraemia is usefully classified as hypovolaemic, normovolaemic and hypervolaemic types

Diagnosis and Assessment The underlying aetiology will remain unknown in about 50% of cases of hyponatraemia Correct management can be instituted if hyponatraemia is correctly classified, whatever the aetiology

Diagnosis and Assessment To correctly classify hyponatraemia it is necessary to: Take a history Establish if vascular volume is increased, reduced or normal Interpret the results of relevant laboratory investigations in the light of the above

Hyponatreamia? Plasma osmolality  2.[Na + ] + 2.[K + ] + [Urea] + [Glucose] Osmolality can be effective or ineffective Serum osmolality? Pseudohyponatraemia ‘ Drip’ artefact Normal or Raised Hyperglycaemia Mannitol therapy Radiographic contrast

Pseudohyponatraemia Normo-osmolar Hyponatraemia Normal Pseudohyponatraemia 7% 20% 93% 80% [Na + ] plasma water: 150 mmol/l 150 mmol/l [Na + ] whole plasma: 140 mmol/l 120 mmol/l Non-aqueous phase Aqueous phase

Renal sodium losses GI fluid losses Skin fluid losses Haemorrhage Heart failure Liver failure Nephrotic syndrome SIADH Other causes of renal water retention Hyponatreamia? True Hyponatreamia Low Increased Normal Reduced Volume status? Serum osmolality? Pseudohyponatraemia ‘ Drip’ artefact Normal or Raised Hyperglycaemia Mannitol therapy Radiographic contrast

Management of Hyponatraemia True Hyponatreamia Correct underlying cause Resuscitate with 0.9% saline Optimise treatment of underlying disease Restrict salt and water Diuretics Specific treatment for non-SIADH states or for SIADH Increased Normal Reduced Volume status?

Causes of Dilutional Hyponatraemia Renal insensitivity to ADH suppression Renal failure ACTH deficiency Thyroid failure Reset osmostat - K + deficiency Non-osmotic ADH secretion SIADH

Criteria for Diagnosis of SIADH Hypo-osmolar hyponatraemia Clinical euvolaemia Osmolality (urine) > Osmolality (plasma) [Na + ] (urine) > 30 mmol/l Normal renal function No deficiency of cortisol or thyroxine No non-osmotic cause for ADH secretion

Management of SIADH Correct underlying cause Residual mild hyponatraemia (Na >125 mmol/l) can be left untreated Water restriction 500-1000 ml/day Demeclocycline 600 mg/day

Management of Non-SIADH Dilutional Hyponatraemia Renal insensitivity to ADH suppression Renal failure ACTH deficiency Thyroid failure Reset osmostat - K + deficiency Non-osmotic ADH secretion

Severe Symptomatic Hyponatraemia Patients suffer double jeopardy of a pressure cone on one hand and CPM on the other Rapid correction is indicated with hyponatraemia known to be acute (12-24 hours), or in the presence of neurological symptoms Otherwise serum sodium correction should be limited to no more than 0.5 mmol/l/hour in the first 48 hours

Is Serum [Na + ] < 125 mmol/l? Neurological symptoms? Duration of hyponatraemia? Yes Chronic hyponatraemia Yes No Emergency correction with 3% saline 1-2 ml/kg/hour until [Na] > 125 mmol/l Urgent correction with 3% saline 1-2 ml/kg/hour until symptoms resolve, continue at 0.5 mmol/l/hour thereafter <24 h >24 h or unknown Routine assessment and management No Adverse outcome unlikely

Hypertonic Saline Therapy Start with 3% saline at 100 ml/hour 100 ml of 3% saline can be expected to increase serum [Na + ] by 2 mmol/l Formulae to estimate the correction doses of iv saline are unreliable Titrate the infusion rate on the basis of hourly serum [Na + ] measurements

Problems Over-reliance on laboratory data Misclassification leading to the over-diagnosis of SIADH Inappropriate application of therapies Inadequate clinical supervision and laboratory monitoring

Future Treatments Vasopressin (V2) receptor antagonists: Highly effective in SIADH and volume expanded hyponatraemia Standard rules for correction rates apply Hyponatraemia relapses on cessation Phenomenally expensive

Hyponatreamia

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Hyponatreamia