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

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

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

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Hyponatreamia

by PeninsulaEndocrine on Nov 11, 2009

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Hyponatreamia — Presentation Transcript