Sodium is the most abundant cation in extracellular fluid and accounts for 90% of plasma osmotic activity. Normal sodium levels are 130-145 mEq/L. Hyponatremia is defined as sodium <130 mEq/L and is classified as mild, moderate or severe based on sodium levels. Hypernatremia is defined as sodium >145 mEq/L. Causes, clinical features, and management of hypo- and hypernatremia are discussed. Slow correction of sodium levels is important to avoid complications.

5. •99% of filtered Na is reabsorbed
•Na is the most abundant cation in ECF.
•Accounts for 90% of osmotic activity in plasma and
ISF.
•Urinary output range from 1 mEq/day on low salt
diet to 400 mEq /day in high salt diet.

6. Sodium - < 130 meq/l
Mild : 130 to 138
Moderate : 120 to 130
Severe :<120
Severe
Acute : <100 meq/l
Chronic : <115meq/l
Types
I
•Acute:
•Chronic
II
•Hypervolaemic hyponatremia
•Hypovolemic hyponatremia
•Normovolemic hyponatremia
•Pseudo hyponatremia

7. Hypervolaemic hyponatremia:
•Absorption of fluid into intravascular compartment.
•Severe : S Na< 100 mmol/l
•Urine sodium will be , 15 mmol /l
Corrected with hypertonic saline.
Slow correction: 2meq/hr
Q4hrly serum sodium measurement

8. Hypovolemic hyponatremia:
Due to:
Diarrhoea & vomiting – urine sodium < 20mmoles/l
Renal causes - urine sodium > 20 mmoles/L
Shock
Correction with isotonic normal saline.

9. Normovolemic Hyponatraemia
Renal failure
SIADH
Treatment:
Fluid restriction.
Demeclocycline – vasopressin anagonist
Pseudohyponatremia
Due to increase in other solutes like glucose,lipids,plasma
protien,urea.

10. Causes of hyponatraemia:
•Intestinal obstruction
•Intestinal fistulas
•Gastric outlet obstruction with vomiting
•Severe diarrhoea
•SIADH
•Immediately after surgery or trauma
•Stroke
•Cerebral salt-wasting syndrome (CSWS) is
a rare endocrine condition featuring a low serum Na
concentration and dehydration in response to
trauma/injury.

11. Clinical features of hyponatraemia:
•Dry coated tongue
•Sunken eyes
•Dry wrinkled skin
•Hypotension
•Dark scanty urine
•Irritability, disorientation.
•Convulsions
Chronic hyponatraemia :
Hypothermia, reduced tendon reflex, pseudo bulbar
palsy.

12. Serum electrolyte. Urine sodium.
Sodium deficit : (125 – present S.sodium) x body
weight(kg) x 0.6
Management:
Acute : Rate 2meq/L/hr
Not more than 10meq /Day
Chronic : Rate < 1 meq/L/hr
Not more than 10 meq/L/day

13. Serum sodium : > 150 meq/L.
Causes:
Normal saline overload
Renal dysfunction
Cardiac failure
Drug induced: NSAIDS,Corticosteroids

14. Clinical features
Pitting oedema
Puffiness of face
Increased urination
Dilated jugular veins
Pulmonary oedema features.

15. Types of Hypernatraemia
Euvolemic :
Failure of water intake – in comatous patient,bedridden ,postoperative,high
fever patient.
Diabetes insipidus
Chronic renal failure.
Hypovolemic:
•More water loss than sodium
•Vomiting
•Diarrhoea
•Undue sweating
•Osmotic diuresis – glucose/mannitol.
Hypervolemic:
•Salt intake
•Hypertonic saline infusion.

16. Restriction of sodium.
Slow correction:
• Dextrose 5%
Fast correction can cause cerebral oedema
Oral / NG administration of water.

17. •5 percent dextrose in water, intravenously, at a rate of 3 to
6 mL/kg per hour.
•The serum sodium and blood glucose should be monitored
every one to two hours until the serum sodium is lowered
below 145 meq/L.
•Once the serum sodium concentration has reached
145 meq/L, the rate of infusion is reduced to
1 mL/kg/hour and continued until normonatremia
(140 meq/L) is restored.
•The goal of this regimen is to lower the serum sodium by
1 to 2 meq/L per hour and to restore normonatremia in less
than 24 hours.
•Free water deficit correction.