2. INTRODUCTION
Euvolemic Hyponatremia is considered in
patients with hyponatremia whose volume
is neither contracted nor expanded and who
are at least by clinical
assessment,euvolemic.
most common in Hospitalized patients
4. HYPOTHYROIDISM
Hypothyroidism results in impaired water excretion leading
to hyponatremia
Pathogenesis:
1.decrease in renal plasma flow and GFR causes
decreased delivery of filtrate to diluting segment
2.persistent secretion of AVP
-Readily reversible by hormonal replacement.
9. SIADH
Serum hypo osmolality and inappropriate urine
concentration (>100mOsm/kgH20) due to inappropriate,
continued secretion or action of AVP despite normal or
increased plasma volume.
Most common cause of hyponatremia in hospitalized
patients
11. PATHOGENESIS
Release of AVP is not inhibited by decreased
plasma osmolality
Enhanced water reabsorption ,leading to
dilutional hyponatremia
Transient expansion of extracellular volume
resulting in release of natriuretic peptide
causing natriuresis
12. CLINICAL FEATURES
Depends on the rate of development
Range from asymptomatic to seizures and coma.
Headache
Drowsiness
Irritability
Seizures
13. DIAGNOSTIC CRITERIA
Essential :
decreased effective osmolality of the extracellular
fluid (Posm<275 mOsm/kg H20)
inappropriate urinary concentration
(Uosm>100mOsm/kg H20
clinical euvolemia
elevated urinary sodium excretion while on a normal
salt and water intake
absence of other potential causes of euvolemic hypo
osmolality.
14. supplemental:
abnormal water load test
plasma AVP level inappropriately elevated relative to
plasma osmolality
no significant correction of serum sodium with
volume expansion but improvement after fluid
restriction
15. MANAGEMENT
Treatment of the cause
1. Drug induced-Cessation of the offending drugs
2. Hypothyroidism, glucocorticoid deficiency -
Hormone replacement
16. Three factors should be taken into consideration when
making a treatment decision for hypoosmolar patient
1) Severity of hyponatremia
2) duration of hyponatremia
3)patient’s neurologic symptomatology
17. Water restriction limited to 500 to 1000 ml /day
Vaptans – Vasopressin receptor antagonist
Conivaptan: only iv preparation
given as 20mg loading dose over 30 mins followed by
continous infusion of 20-40mg/day
18. Tolvaptan: an oral AVPR antagonist
starting dose is 15 mg on first day and the dose can
be titrated to 30mg and 60 mg at 24 hrs interval if
serum Na+ remains <135mEq/L or increase in serum
sodium <5mEq/L in the previous 24 hrs
19.
20. recommended maximum limit of correction: 12mEq/l in
24 hrs or 18 mEq/l in 48 hrs
patients with high risk of ODS
Severely low sodium <105mEq/L
malnutrition
alcoholism
liver disease
hypokalemia
the correction should not be more than
8mEq/L in 24 hrs
21. Osmotic demyelination syndrome
Involves both pontine and extra-pontine
myelinolysis (EPM)
Pathophysiology
a reduced adaptive capacity of the neuroglia to
large shifts in the serum osmolarity
the cellular edema caused by fluctuations in
electrolytes results in compression and
subsequent demyelination of fiber tracts.
22. Clinical features
a rapid recovery of hyponatremia with
normalization of serum sodium followed by
deterioration.
correlates with a rapid correction of serum
sodium levels.
Pons along with corticobulbar and corticospinal
tract- dysarthria and dysphagia along with flaccid
paralysis changing over to spastic later on.
EPM - tremor, ataxia and movement disorders
like mutism, Parkinsonism, dystonia,etc.
23. Management of rapid correction of
hyponatremia
stop all active therapies including saline infusion and
pharmacological therapies
give water orally or iv as 5%dextrose at a volume that
hourly equals urine output
desmopressin:1-2mcg sc
24. Long term treatment of chronic
hyponatremia
Some patients may require long term therapy
based on the etiology of SIADH
Tolvaptan can be used for continued daily
therapy for as long as 4 years.
A reasonable period of tolvaptan cessation to
evaluate the presence of continued SIADH is 7
days.
