HYPONATREMIA
Dr. Nishat Tasnim
Resident (Phase A: Oncology)
Internal Medicine (Violet Unit)
Overview
• Introduction
• Types of Hyponatremia
• Etiology with Pathogenesis
• Clinical Features
• Diagnosis
• Management
• Osmotic Demyelination Syndrome
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.
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.
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.
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}
Hypotonic Hyponatremia
Pathogenesis: Diuretic Therapy
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 +.
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)
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.
Gastrointestinal and Third-Space
Sequestered Losses
SIADH (Syndrome of Inappropriate ADH
Secretion)
• A defect in osmoregulation
causes vasopressin to be
inappropriately stimulated,
leading to urinary
concentration.
Cardiac Failure
Liver Cirrhosis
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.
Diagnostic Approach
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
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.
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
• 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
• 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)
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
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
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).
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
• 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].
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
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.
Hyponatremia

Hyponatremia

  • 2.
    HYPONATREMIA Dr. Nishat Tasnim Resident(Phase A: Oncology) Internal Medicine (Violet Unit)
  • 3.
    Overview • Introduction • Typesof 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 asserum 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.
  • 7.
    Isotonic hyponatremia • Expansionof 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 • Seenwhen 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}
  • 9.
  • 11.
  • 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 • Excretionof 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 WastingSyndrome • 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.
  • 15.
  • 16.
    SIADH (Syndrome ofInappropriate ADH Secretion) • A defect in osmoregulation causes vasopressin to be inappropriately stimulated, leading to urinary concentration.
  • 18.
  • 19.
  • 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.
  • 22.
  • 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 toguide 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 mildsymptoms @ 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 areavailable 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 kgfemale 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 slowlydeveloping 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 hypovolemichyponatremia • 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 euvolemichyponatremia • 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- Glucocorticoidreplacement 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 ODSoccurs 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
  • 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.