3. Overview
• Introduction
• Types of Hyponatremia
• Etiology with Pathogenesis
• Clinical Features
• Diagnosis
• Management
• Osmotic Demyelination Syndrome
4. Introduction
• Sodium (Na) is the major cation of ECF.
• Total body Na> 5000mEq of which 85-90% extra cellular.
• Responsible for >90% total osmolarity of ECF.
• Maintain ECF volume hence Blood pressure.
• Daily requirement >100mEq or 6gm salt.
5. Hyponatremia
• Defined as serum sodium below 135 mmol/L.
• Most common disorder of electrolytes encountered in clinical
practice, occuring in 25 - 30% of hospitalized patients.
• Independent predictor of mortality.
• Basically a water imbalance.
6.
7. Isotonic hyponatremia
• Expansion of extracellular fluid with isotonic fluids that do not contain
Na, here is no transcellularshift of water but the [Na+] decreases
Ex- Hypertriglyceridemia
Hyperproteinemia( as in Multiple Myeloma)
• Rise in plasma lipids of 4.6 g/L or plasma protein concentrations
greater than 10 g/dL will decrease the sodium concentration by
approximately 1 mEq/L.
8. Hypertonic hyponatremia
• Seen when there is increase in effective osmoles in the extracellular
fluid.
• Shift of water from the cells to the ECF and thus causing
translocational hyponatremia
Ex- Hyperglycaemia in DM {plasma Na + falls by 2 mEq/l for
every 100-mg/dL increase in Glucose; and by 4 mEq/l at Glucose >
400mg/dl}
12. Mineralocorticoid (Aldosterone) Deficiency
• Characterized by hyponatremia with ECF volume contraction.
• Hypotensive and/or hypovolemic patient present with Urine [Na + ]
above 20 mmol/l, and high serum K +.
13. Osmotic diuresis
• Excretion of osmotically active nonreabsorbable or poorly
reabsorbable solute
Glycosuria
Ketonuria (e.g., in starvation or in diabetic or alcoholic ketoacidosis)
Bicarbonaturia (e.g., in renal tubular acidosis or metabolic alkalosis,
in which the associated bicarbonaturia leads to loss of Na)
14. Cerebral Salt Wasting Syndrome
• Is a syndrome described following SAH, head injury, or neurosurgical
procedures, as well in other settings.
• Primary defect is salt wasting from the kidneys with subsequent
volume contraction, which stimulates vasopressin release.
• Uncommon.
16. SIADH (Syndrome of Inappropriate ADH
Secretion)
• A defect in osmoregulation
causes vasopressin to be
inappropriately stimulated,
leading to urinary
concentration.
20. Chronic Kidney Disease
• Urine output is relatively fixed and water intake in excess of urine
output and insensible losses will cause hyponatremia.
• Edema usually develops when the Na + ingested exceeds the kidneys
capacity to excrete.
24. Investigations
• Serum osmolarity, Na, K
• BUN and creatinine
• Serum glucose, uric acid
• Urine Na, K, Osmolarity
• Serum proteins & Lipid profile
• Thyroid, adrenal, and pituitary function
• Radiology
Chest X Ray - PA view
CT scan of Thorax & Brain
25. Management
Major considerations to guide therapy for hyponatremia includes
• Rate of development of symptoms
• Severity of symptoms
• Risk for Osmotic Demyelination Syndrome
Once the urgency of correcting the plasma Na + concentration has
been established and appropriate therapy instituted, the focus should
be on treatment or withdrawal of the underlying cause.
26. Acute Symptomatic hyponatremia
• Medical emergency.
• Rate of correction: 1.5-2 meq/l/h for the first 3-4 hours; total 8-12
meq/l/day
• Na + deficit = 0.6 x body weight x (target Na + conc – starting Na +
conc).
• Hypertonic saline (3% NaCl) @ 1-2 ml/kg/hour
27. • For mild symptoms @ 0.5 ml/kg/hour + lasix 20-40 mg IV
• For seizures & coma @ 2-4 ml/kg/hour + lasix 20-40 mg IV
• Monitored every 2–4 h
28. • Equations are available to help calculate the initial rate of fluids to be
administered.
• A widely used formula is the Adrogue-Madias formula
• Change in serum Na+ with infusing solution=
[infusate Na]-serum Na / (total body water +1)
• Infusate Na+ is the [Na+] in the infused fluid (154meq/l in 0.9%NS,
513meq/l in 3%NS, 77meq/l in 0.45%NS)
29. For example,
60 kg female with Na- 110 m Eq/l.
• Correction using 3% NaCl (513 mEq/l) – (513-110 ) / 30 +1 = 400 /31 =
13 mEq/l
• So infusion of 1 L of 3% NaCl in this patient will raise Na by 13 mEq/l.
• Since correction to be done at 2 mEq/hr, 1 litre of 3% NaCl should be
infused over 6.5 hrs. i.e. @ 40 drops/min
30. Chronic or slowly developing
hyponatremia
• Correction rate should be 0.5 meq/l/h , total 8-12 meq/l/day or
• < 10 mMol in 1 st 24 hrs, < 18 mMol in 48 hrs
31. Treatment of hypovolemic hyponatremia
• Diuretic related-
Discontinuation of thiazides and correction of volume deficits.
• Mineralocorticoid deficiency-
Volume repletion with isotonic saline, Fludrocortisone
chronically for mineralocorticoid replacement (if needed).
32. Treatment of euvolemic hyponatremia
• SIADH-
For most cases of mild-to moderate SIADH, fluid restriction
represents the cheapest and least toxic therapy. (fluid restriction 500
mL/d below the 24-hour urine volume.
Failure to water restriction
- Vaptans
- Democlocycline 150- 300 mg PO tid or qid
- Fludrocortisone 0.05-0.2 mg bid
33. • Glucocorticoid Deficiency-
Glucocorticoid replacement at either maintenance or stress
doses, depending on the degree of intercurrent illness.
• Severe Hypothyroidism-
Thyroid hormone replacement at standard weight-based doses;
several days may be needed to normalize the serum [Na].
34. Osmotic Demyelination Syndrome
ODS occurs if chronic hyponatremia is corrected too rapidly.
• Present in a stereotypical biphasic pattern (initially improve neurologically
with correction of hyponatremia, but then, one to several days later, new,
progressive, and sometimes permanent neurological deficits emerge).
• Patients can present para- or quadraparesis, dysphagia, dysarthria, diplopia, a
"locked-in syndrome," and/or loss of consciousness.
• Most commonly affected area is pons
35.
36.
37. Take Home Message
• Hyponatremia is a common electrolyte abnormality in day to day
practice, so we should look for it carefully.
• While managing a case, appropriate rate and optimal method of
sodium correction is necessary.