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Presenter: Dr. Mohammad Rehan
Hyponatremia
Contents
• Basic physiology
• Introduction
• Etiology
• Clinical manifestations
• Approach
• Treatment
• Case discussion
Basic Physiology
1. Water regulation
In a normal person water in body is balanced by adjustment in
input and urine output
A. Response to water deficit
Water intake is regulated by thirst, the stimuli for which are :
i. Dehydration
ii. Fall in BP
iii. Increased solute conc.( osmolality)
Water excretion is tightly regulated by ADH
As much as 18 L of water can be absorbed by ADH
B. Response to water excess
• Decrease ADH
• Increase ANP
So in conclusion decreased ADH and increased ANP will decrease water
reabsorption and increase urine output and thereby maintain req. water
status in body
amount of water in body ADH secretion
Water reabsorption by CTUrine Volume
Volume Expansion ANP secretion
Natriuresis and Diuresis
1. Sodium Regulation
A. Physiology
i. Sodium is the major ECF cation(140 mEq/L)
ii. Total body Na is about 5000 mEq in a normal adult person
iii. 85-90% Na is extracellular
iv. It is responsible for >90% of total osmolality of ECF
v. Major function is to maintain ECF volume and therefore maintain BP
vi. ECF volume is the reflection of Total body Na content
vii. Daily requirement of Na is about 100 mEq or 6 gm of NaCl
viii. Excess salt is excreted chiefly by kidneys
A. Response to Na deficit
i. Deficiency of Na in body will lead to hypovolemia and activates
Angiotensin-2 and Aldosterone
ii. Angiotensin-2 : increase Na absorption at PCT
Aldosterone : increase Na absorption at CD
B. Response to Sodium Excess
i. Increased ECF volume decreased Aldosterone and Angiotensin 2 and
Increased ANP
Natriuresis Renal reabsorption of Na
and Diuresis
Introduction
 Defined as a serum [Na] below 135 mmol/L.
 Most common disorder of electrolytes encountered in
clinical practice, occurring in 22% of hospitalized
patients.
Important clinically because:
1) Acute severe hyponatremia can cause substantial
morbidity and mortality;
2) Adverse outcomes are higher in hyponatremic
patients with a wide range of underlying diseases;
3) Overly rapid correction of chronic hyponatremia can
cause severe neurological deficits and death.
Hyponatremia = Sodium deficit
So salt requirement is required in all
This is a WRONG CONCEPT
Hyponatremia usually means WATER
RETENTION
Etiology
Based on 2 criterias- Osmolality and ECF volume
1. Pseudo Hyponatremia
i. Normal Osmolality- hyperlipidaemia, hyperproteinaemia
ii. High Osmolality – hyperglycaemia, mannitol
2. True Hyponatremia( Hypo-osmolar)
i. Hypovolumic
ii. Euvolumic
iii. Hypervolumic
ETIOLOGIES AND PATHOPHYSIOLOGIES OF
HYPOTONIC HYPONATREMIAS
Hypovolemic Hyponatremia(↓H2O,↓↓Na+)
Vomiting or
Diarrhoea
Burns
Peritonitis
Bowel lumen ileus
Loss water &
Na+, Cl--
free water or hypotonic
fluid intake
Gastrointestinal and Third-Space
Sequestered Losses
Hypovolemic
hyponatremia
Vasopressin
due to volume
contraction
Loop diuretics
In TALH
Blocks
sodium
reabsorption
Interferes with the
generation of a
hypertonic medullary
interstitium
Thiazide diuretics
DCT
Interfering with urinary
dilution rather than with
urinary concentration
More free water
excretion, inspite
of vasopressin
Limits free water
excretion
Diuretic therapy
 Is a syndrome described following SAH, head injury, or
neurosurgical procedures, as well in other settings.
 Primary defect is salt wasting from the kidneys(?role
of BNP) with subsequent volume contraction, which
stimulates vasopressin release.
 Uncommon.
Cerebral Salt Wasting syndrome
 Characterized by hyponatremia with ECF
volume contraction (provides the nonosmotic
stimulus for vasopressin release).
 Urine[Na+] above 20 mmol/l, and high serum
K+.
Mineralocorticoid (Aldosterone) Deficiency
Euvolemic Hyponatremia(↑H2O, ←→Na+)
• A defect in osmoregulation causes vasopressin to be
inappropriately stimulated, leading to urinary concentration.
• MCC of euvolumic hyponatremia
• Excess vasopressin: CNS disturbances such as hemorrhage,
tumors, infections, and trauma.
• Ectopic vasopressin: Small cell lung cancers, cancer of the
duodenum and pancreas, and olfactory neuroblastoma.
• Idiopathic: seen in elderly(10%).
SIADH (Syndrome of Inappropriate ADH Secretion)
Criteria for Diagnosing SIADH
• Decreased effective osmolality of the extracellular fluid.
• Inappropriate urinary concentration (Uosm >100 mOsmol/kg
H2O) with normal renal function) at some level of plasma
hypo- osmolality.
• Clinical euvolemia.
• Elevated urinary sodium excretion (>20 mmol/L) while
on normal salt and water intake.
• Absence of other potential causes of euvolemic hypo-
osmolality
• Normal renal function and absence of diuretic use,
particularly thiazide diuretics.
Supporting diagnostic criteria for SIADH
• Serum uric acid <4 mg/dL
• Blood urea nitrogen <10 mg/dL
• Fractional sodium excretion >1%; fractional urea
excretion >55%
• Failure to improve or worsening of hyponatremia after
0.9% saline infusion
• Improvement of hyponatremia with fluid restriction
Posterior pituitary
Vasopressin
glucocor
─ticoids
Severe
hypothyroidism
(myxedema coma)
↓CO
↓GFR,
↑vasopressin
Psychogenic
polydipsia
*↑Thirst perception,
*Acute psychosis
secondary to
schizophrenia, Anxiety
*Often on SSRI’s,
*CT or MRI to r/o CNS
sarcoidosis and
craniopharyngioma.
Postoperative
hyponatremia
• Excessive infusion of free
water (5% dextrose) and
• ↑Vasopressin due to pain
Exercise-Associated
Hyponatremia(EAH)
•Long-distance marathon runners.
increased risk:
•BMI below 20 kg/m2,
•Running time exceeding 4 hours
•Consumption of fluids every mile
↑vasopressin
Drugs that enhance vasopressin release
Clofibrate
Carbamazepine
Vincristine
Nicotine
Narcotics
SSRI
ifosfamide
Vasopressin analogues
Desmopressin
Oxytocin
Drugs that potentiate renal action of
vasopressin
Cyclophosphamide
NSAIDs
Acetaminophen
Drugs that cause hyponatremia by
unknown mechanisms
Haloperidol
Amitryptyline
Fluoxetine
Fluphenazine
IVIG
Methylmethamphetamine (MDMA)
Drugs Causing Hyponatremia
Hypervolemic Hyponatremia (↑↑H2O, ↑Na+)
Failure
↓MAP, ↓CO
Reduced effective
intravascular volume
↑vasopressin
(non osmotic baroreceptor
stimulation)
↑Norepinephrine
↓GFR
RAAS
↑Thirst
↑plasma renin,
↑ norepinephrine,
↑ vasopressin
↓GFR, ↑free water retention
Dilutional hyponatremia
Cirrhosis
In pts of advanced cirrhosis
↑extracellular volume (ascites, edema).
↑ plasma volume (splanchnic venous dilation)
Advanced 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.
Clinical Manifestations of Hyponatremia
Acute Hyponatremia – <48 hours
chronic hyponatremia - > 48 hours
STEP 1 – Serum
Osmolalit
y
Serum Osmolality: lab value or
calculation – in mosm/kg
=(2 x Na+) + (glucose/18) + (BUN/2.8)
Hypertonic - >295
hyperglycemia, mannitol, glycerol
Isotonic - 280-295
pseudo-hyponatremia from elevated lipids or
protein
Hypotonic - <280
excess fluid intake, low solute intake, renal
disease, SIADH, hypothyroidism, adrenal
insufficiency, CHF, cirrhosis, etc.
STEP 2 –Volume
Statu
s
2ndassess volume status (extracellular fluid volume)
Hypotonic hyponatremia has 3 main etiologies:
Hypovolemic – both water and Na decreased (H20 <
Na)
Consider obvious losses from diarrhea,
vomiting, dehydration, malnutrition, etc
Euvolemic – water increased and Na stable
Consider SIADH, thyroid disease, primary
polydipsia
Hypervolemic – water increased and Na increased
(H2O > Na)
Consider obvious CHF, cirrhosis, renal failure
STEP 3 – Urine
Studie
s
For euvolemic hyponatremia, check urine osmolality
Urine osmolality <100 - excess water intake
Primary polydipsia, tap water enemas, post-TURP
Urine osmolality >100 - impaired renal concentration
SIADH, hypothyroidism, cortisol deficiency
Check urine sodium & calculate FeNa %
Low urine sodium (<20) and low FeNa (<1%)
implies the kidneys are appropriately reabsorbing
sodium
High urine sodium (>20) and high FeNa (>1%)
implies the kidneys are not functioning properly
Treatment
When considering the treatment of patients with
hyponatremia, five issues must be addressed:
• Risk of osmotic demyelination
• Appropriate rate of correction to minimize this risk
• Optimal method of raising the plasma
sodium concentration
• Estimation of the sodium deficit if sodium is to
be given
• Management of the patient in whom overly
rapid correction has occurred
General principles of treatment
Primarily determined by the severity of symptoms and
the cause of the hyponatremia
• Symptomatic hyponatremia (seizures, or coma)
o likely to occur with an acute case and marked
reduction in the plasma sodium concentration
o Aggressive therapy is required.
o Chronic but significant hyponatremia
where less severe neurologic symptoms occur
fatigue, nausea, dizziness, gait disturbances,
confusion, lethargy, and muscle cramps
These symptoms typically do not mandate
aggressive therapy
Methods of Sodium Correction
• Water restriction
• primary therapy for hyponatremia in edematous states,
SIADH, primary polydipsia, and advanced renal failure.
• Sodium chloride administration
•
• usually as isotonic saline or increased dietary salt
given to patients with true volume depletion, adrenal
insufficiency, and in some cases of SIADH.
contraindicated in edematous patients (eg, heart
failure, cirrhosis, renal failure) since it will lead to
exacerbation of the edema
•Hypertonic saline is generally recommended only for
patients with symptomatic or severe hyponatremia.
• The increase in plasma Na+concentration can be highly
unpredictable during treatment with hypertonic saline due
to rapid changes in the underlying physiology.
• Patient should be monitored carefully for changes in
neurologic and pulmonary status, and serum electrolytes
should be checked frequently, every 2 - 4 hours.
Goal:
• Urgent correction by 1-2 mmol/hr upto 4-6 mmol/L, to
prevent brain herniation and neurological damage
from cerebral ischemia.
• Upper limit for correction,10-12 mmol/L in any 24hour
period; 18 mmol/L in any 48-hour period.
Treatment of symptomatic acute hyponatremia
how much fluids to give?
Total body water = weight x 0.6 for men / 0.5 for woman
• One liter of NS contains: 154 mmol/L of Na+ Cl−
• One liter of 3% saline contains:513 mmol/L of Na+ Cl−
Example: An 60-kg man is having seizure .His
s.Na is 110 mmol /L.
Means of correction:
Given the acuity, the patient should be given
hypertonic saline, which has 513 mmol of Na per
liter.
{513 - 110} /{60 x 0.6 +1}= 10
mmol/LOne liter of this fluid would increase Na by 10
mmol/L.
Dose of hypertonic saline
at 200 mL/hr until symptoms improve.
Maximum 1 litre of 3% NS should be given
in 24 hour.
Goal:
Minimum correction of serum [Na] by 4-8 mmol/L per
day, with a lower goal of 4-6 mmol/L per day if the risk of
ODS is high.
Limits not to exceed:
• 8-10 mmol/L in any 24-hour period.
Treatment of chronic hyponatremia(Avoiding
ODS)
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.
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
- Demeclocycline 150- 300 mg PO tid or qid
-Fludrocortisone 0.05-0.2 mg bid
Treatment of euvolemic hyponatremia
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].
HeartFailure- for patients with mild to moderate
symptoms, begin with fluid restriction (1 L/d total) and, if
signs of volume overload are present, administer loop
diuretics.
If the serum [Na] does not correct to the desired level, lift the
fluid restriction and start either conivaptan or tolvaptan.
Treatment of hypovolemic hyponatremia
Cirrhosis-Severe daily fluid restriction,
Vaptans an alternative choice if fluid restriction has failed to maintain
a serum [Na] 130 mmol/L; however, tolvaptan use should be
restricted to cases where the potential clinical benefit outweighs the
risk of worsened liver function, such as in patients with end-stage
liver disease and severe hyponatremia who are awaiting imminent
liver transplantation.
CKD-Restricting fluid intake. Aquaretics (vaptans)
can be employed{not be expected to cause a
clinically significant aquaresis with severe renal
impairment (ie, serum creatinine >2.5 mg/dL)}.
Role of VAPTANS
Vaptans have long been anticipated as a more effective
method to treat hyponatremia by virtue of their unique effect
to selectively increase solute-free water excretion by the
kidneys.
Although not C/I with decreased renal function, these
agents generally will not be effective if S.Cr is >2.5mg%.
Conivaptan Tolvaptan Lixivaptan
Receptor V1a/V2 antagonist V2 antagonist V2 antagonist
Route i.v Oral Oral
Urine volume ↑ ↑ ↑
Urine
osmolality
↓ ↓ ↓
Sodium
excretion/d
↔ ↔ ↔ at low dose,
↑at high dose
Status FDA approved FDA & EMAapproved Phase 3
completed
Dosage 20mg over 30min f/b cont
inf 20-40mg/d
15mg on D1, then titrate to
30-60mg/d
-
Duration of
treatment
Max 4days (interaction with
CYP3A4)
≤30days(risk of hepatic
injury)
-
Side effects Headache, thirst,
hypokalemia
Drymouth, thirst, dizziness,
hypotension
-
Indications Euvolumic and
hypervolumic hyponatremia
Euvolumic and hypervolumic
hyponatremia
-
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.
• Other regions of the brain affected in ODS: (in order of
frequency) cerebellum, lateral geniculate body, thalamus,
putamen, and cerebral cortex or subcortex.
• As these lesions may not appear until 2 weeks after development, a diagnosis
of myelinolysis should not be excluded if the imaging is initially normal.
Starting serum [Na] ≥120 mmol/L: Intervention unnecessary.
Starting serum [Na] <120 mmol/L:
Withhold the next dose of vaptan if the correction is >8
mmol/L;
Consider therapeutic re-lowering of serum [Na] if
correction exceeds therapeutic limits;
Consider administration of high-dose glucocorticoids (eg,
dexamethasone, 4 mg every 6 hrs) for 24-48hrs following
the excessive correction.
Managing excessive correction of chronic hyponatremia
Re-lowering serum [Na]:
Administer desmopressin to prevent further water losses:
2-4 mg every 8 hours parenterally;
Replace water orally or as 5% dextrose in water
intravenously: 3 mL/kg/h;
Recheck serum [Na] hourly and continue therapy infusion
until serum [Na] is reduced to goal
Hypotonic
hyponatremia/tru
e hyponatremia
Pseudohyponatremia/osmotic
related
Primary renal
disease
Impaired renal
function
Access
volume
status
Access
renal
status
Normal
Volume
depletion
Edema – CHF, cirrhosis, nephrotic
syndrome
Ur, Na + <20 =
diarrhoea,
vomiting, burns,
pancreatitis
Ur, Na + >20 = diuretics,
salt losing
nephropathy
Normal
volume
Adrenal &
thyroid
function
Adrenal & thyroid
insufficiency
Normal
Access Urine
osmolality(Abl
e to dilute
urine)
>100 mOsmol/kg
Dilute
urine
Psychogenic
polydipsia
NO
YES
Access serum osmolality
low
Normal/high
SIAD
Approach to a case of hyponatremia
Case Discussion
 74-year-old man p/w recent gastroenteritis characterized by
n/v/d x 5 days, in addition to fatigue and headache.
 CT head (-) in ED. No focal neurologic deficits found. He looks dry
on physical exam, with no evidence of fluid overload.
 BMP significant for Na+ of 118, baseline unknown. Serum
osmolality is 266. Urine osmolality is 377. Urine sodium is 8.
 How would you approach this patient’s hyponatremia?
 How would your approach be different if this patient presented with
new-onset seizures?
74-year-old man p/w recent gastroenteritis characterized by n/v/d x
5 days, in addition to fatigue and headache.
BMP significant for Na+ of 118, baseline unknown. Serum osmolality
is 266. Urine osmolality is 377.
How would you approach this patient’s hyponatremia? The steps:
1) Serum osmolality – 266, decreased (hypotonic)
2) Urine osmolality –377, increased (>100)
3) Volume status – hypovolemic
4) Urine Na, FeNa – urine Na 8, appropriately reabsorbing, likely
volume depleted 2/2 N/V
5) Treatment: Mild symptoms, correct slowly w/ isotonic saline
How would your approach be different if this patient presented
with new-onset seizures?
For symptomatic, severe hyponatremia, more rapid
correction using 3% normal saline
THANK YOU

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Hyponatremiappt 170315180214

  • 1. Presenter: Dr. Mohammad Rehan Hyponatremia
  • 2. Contents • Basic physiology • Introduction • Etiology • Clinical manifestations • Approach • Treatment • Case discussion
  • 3. Basic Physiology 1. Water regulation In a normal person water in body is balanced by adjustment in input and urine output A. Response to water deficit Water intake is regulated by thirst, the stimuli for which are : i. Dehydration ii. Fall in BP iii. Increased solute conc.( osmolality) Water excretion is tightly regulated by ADH As much as 18 L of water can be absorbed by ADH
  • 4. B. Response to water excess • Decrease ADH • Increase ANP So in conclusion decreased ADH and increased ANP will decrease water reabsorption and increase urine output and thereby maintain req. water status in body amount of water in body ADH secretion Water reabsorption by CTUrine Volume Volume Expansion ANP secretion Natriuresis and Diuresis
  • 5. 1. Sodium Regulation A. Physiology i. Sodium is the major ECF cation(140 mEq/L) ii. Total body Na is about 5000 mEq in a normal adult person iii. 85-90% Na is extracellular iv. It is responsible for >90% of total osmolality of ECF v. Major function is to maintain ECF volume and therefore maintain BP vi. ECF volume is the reflection of Total body Na content vii. Daily requirement of Na is about 100 mEq or 6 gm of NaCl viii. Excess salt is excreted chiefly by kidneys
  • 6. A. Response to Na deficit i. Deficiency of Na in body will lead to hypovolemia and activates Angiotensin-2 and Aldosterone ii. Angiotensin-2 : increase Na absorption at PCT Aldosterone : increase Na absorption at CD B. Response to Sodium Excess i. Increased ECF volume decreased Aldosterone and Angiotensin 2 and Increased ANP Natriuresis Renal reabsorption of Na and Diuresis
  • 7. Introduction  Defined as a serum [Na] below 135 mmol/L.  Most common disorder of electrolytes encountered in clinical practice, occurring in 22% of hospitalized patients.
  • 8. Important clinically because: 1) Acute severe hyponatremia can cause substantial morbidity and mortality; 2) Adverse outcomes are higher in hyponatremic patients with a wide range of underlying diseases; 3) Overly rapid correction of chronic hyponatremia can cause severe neurological deficits and death.
  • 9. Hyponatremia = Sodium deficit So salt requirement is required in all This is a WRONG CONCEPT Hyponatremia usually means WATER RETENTION
  • 10. Etiology Based on 2 criterias- Osmolality and ECF volume 1. Pseudo Hyponatremia i. Normal Osmolality- hyperlipidaemia, hyperproteinaemia ii. High Osmolality – hyperglycaemia, mannitol 2. True Hyponatremia( Hypo-osmolar) i. Hypovolumic ii. Euvolumic iii. Hypervolumic
  • 11. ETIOLOGIES AND PATHOPHYSIOLOGIES OF HYPOTONIC HYPONATREMIAS
  • 13. Vomiting or Diarrhoea Burns Peritonitis Bowel lumen ileus Loss water & Na+, Cl-- free water or hypotonic fluid intake Gastrointestinal and Third-Space Sequestered Losses Hypovolemic hyponatremia Vasopressin due to volume contraction
  • 14. Loop diuretics In TALH Blocks sodium reabsorption Interferes with the generation of a hypertonic medullary interstitium Thiazide diuretics DCT Interfering with urinary dilution rather than with urinary concentration More free water excretion, inspite of vasopressin Limits free water excretion Diuretic therapy
  • 15.  Is a syndrome described following SAH, head injury, or neurosurgical procedures, as well in other settings.  Primary defect is salt wasting from the kidneys(?role of BNP) with subsequent volume contraction, which stimulates vasopressin release.  Uncommon. Cerebral Salt Wasting syndrome
  • 16.  Characterized by hyponatremia with ECF volume contraction (provides the nonosmotic stimulus for vasopressin release).  Urine[Na+] above 20 mmol/l, and high serum K+. Mineralocorticoid (Aldosterone) Deficiency
  • 18. • A defect in osmoregulation causes vasopressin to be inappropriately stimulated, leading to urinary concentration. • MCC of euvolumic hyponatremia • Excess vasopressin: CNS disturbances such as hemorrhage, tumors, infections, and trauma. • Ectopic vasopressin: Small cell lung cancers, cancer of the duodenum and pancreas, and olfactory neuroblastoma. • Idiopathic: seen in elderly(10%). SIADH (Syndrome of Inappropriate ADH Secretion)
  • 19. Criteria for Diagnosing SIADH • Decreased effective osmolality of the extracellular fluid. • Inappropriate urinary concentration (Uosm >100 mOsmol/kg H2O) with normal renal function) at some level of plasma hypo- osmolality. • Clinical euvolemia. • Elevated urinary sodium excretion (>20 mmol/L) while on normal salt and water intake. • Absence of other potential causes of euvolemic hypo- osmolality • Normal renal function and absence of diuretic use, particularly thiazide diuretics.
  • 20. Supporting diagnostic criteria for SIADH • Serum uric acid <4 mg/dL • Blood urea nitrogen <10 mg/dL • Fractional sodium excretion >1%; fractional urea excretion >55% • Failure to improve or worsening of hyponatremia after 0.9% saline infusion • Improvement of hyponatremia with fluid restriction
  • 21. Posterior pituitary Vasopressin glucocor ─ticoids Severe hypothyroidism (myxedema coma) ↓CO ↓GFR, ↑vasopressin Psychogenic polydipsia *↑Thirst perception, *Acute psychosis secondary to schizophrenia, Anxiety *Often on SSRI’s, *CT or MRI to r/o CNS sarcoidosis and craniopharyngioma.
  • 22. Postoperative hyponatremia • Excessive infusion of free water (5% dextrose) and • ↑Vasopressin due to pain Exercise-Associated Hyponatremia(EAH) •Long-distance marathon runners. increased risk: •BMI below 20 kg/m2, •Running time exceeding 4 hours •Consumption of fluids every mile ↑vasopressin
  • 23. Drugs that enhance vasopressin release Clofibrate Carbamazepine Vincristine Nicotine Narcotics SSRI ifosfamide Vasopressin analogues Desmopressin Oxytocin Drugs that potentiate renal action of vasopressin Cyclophosphamide NSAIDs Acetaminophen Drugs that cause hyponatremia by unknown mechanisms Haloperidol Amitryptyline Fluoxetine Fluphenazine IVIG Methylmethamphetamine (MDMA) Drugs Causing Hyponatremia
  • 25. Failure ↓MAP, ↓CO Reduced effective intravascular volume ↑vasopressin (non osmotic baroreceptor stimulation) ↑Norepinephrine ↓GFR RAAS ↑Thirst
  • 26. ↑plasma renin, ↑ norepinephrine, ↑ vasopressin ↓GFR, ↑free water retention Dilutional hyponatremia Cirrhosis In pts of advanced cirrhosis ↑extracellular volume (ascites, edema). ↑ plasma volume (splanchnic venous dilation)
  • 27. Advanced 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.
  • 29. Acute Hyponatremia – <48 hours chronic hyponatremia - > 48 hours
  • 30. STEP 1 – Serum Osmolalit y Serum Osmolality: lab value or calculation – in mosm/kg =(2 x Na+) + (glucose/18) + (BUN/2.8) Hypertonic - >295 hyperglycemia, mannitol, glycerol Isotonic - 280-295 pseudo-hyponatremia from elevated lipids or protein Hypotonic - <280 excess fluid intake, low solute intake, renal disease, SIADH, hypothyroidism, adrenal insufficiency, CHF, cirrhosis, etc.
  • 31. STEP 2 –Volume Statu s 2ndassess volume status (extracellular fluid volume) Hypotonic hyponatremia has 3 main etiologies: Hypovolemic – both water and Na decreased (H20 < Na) Consider obvious losses from diarrhea, vomiting, dehydration, malnutrition, etc Euvolemic – water increased and Na stable Consider SIADH, thyroid disease, primary polydipsia Hypervolemic – water increased and Na increased (H2O > Na) Consider obvious CHF, cirrhosis, renal failure
  • 32. STEP 3 – Urine Studie s For euvolemic hyponatremia, check urine osmolality Urine osmolality <100 - excess water intake Primary polydipsia, tap water enemas, post-TURP Urine osmolality >100 - impaired renal concentration SIADH, hypothyroidism, cortisol deficiency Check urine sodium & calculate FeNa % Low urine sodium (<20) and low FeNa (<1%) implies the kidneys are appropriately reabsorbing sodium High urine sodium (>20) and high FeNa (>1%) implies the kidneys are not functioning properly
  • 33.
  • 34. Treatment When considering the treatment of patients with hyponatremia, five issues must be addressed: • Risk of osmotic demyelination • Appropriate rate of correction to minimize this risk • Optimal method of raising the plasma sodium concentration • Estimation of the sodium deficit if sodium is to be given • Management of the patient in whom overly rapid correction has occurred
  • 35. General principles of treatment Primarily determined by the severity of symptoms and the cause of the hyponatremia • Symptomatic hyponatremia (seizures, or coma) o likely to occur with an acute case and marked reduction in the plasma sodium concentration o Aggressive therapy is required. o Chronic but significant hyponatremia where less severe neurologic symptoms occur fatigue, nausea, dizziness, gait disturbances, confusion, lethargy, and muscle cramps These symptoms typically do not mandate aggressive therapy
  • 36. Methods of Sodium Correction • Water restriction • primary therapy for hyponatremia in edematous states, SIADH, primary polydipsia, and advanced renal failure. • Sodium chloride administration • • usually as isotonic saline or increased dietary salt given to patients with true volume depletion, adrenal insufficiency, and in some cases of SIADH. contraindicated in edematous patients (eg, heart failure, cirrhosis, renal failure) since it will lead to exacerbation of the edema •Hypertonic saline is generally recommended only for patients with symptomatic or severe hyponatremia.
  • 37. • The increase in plasma Na+concentration can be highly unpredictable during treatment with hypertonic saline due to rapid changes in the underlying physiology. • Patient should be monitored carefully for changes in neurologic and pulmonary status, and serum electrolytes should be checked frequently, every 2 - 4 hours.
  • 38. Goal: • Urgent correction by 1-2 mmol/hr upto 4-6 mmol/L, to prevent brain herniation and neurological damage from cerebral ischemia. • Upper limit for correction,10-12 mmol/L in any 24hour period; 18 mmol/L in any 48-hour period. Treatment of symptomatic acute hyponatremia
  • 39. how much fluids to give? Total body water = weight x 0.6 for men / 0.5 for woman • One liter of NS contains: 154 mmol/L of Na+ Cl− • One liter of 3% saline contains:513 mmol/L of Na+ Cl−
  • 40. Example: An 60-kg man is having seizure .His s.Na is 110 mmol /L. Means of correction: Given the acuity, the patient should be given hypertonic saline, which has 513 mmol of Na per liter. {513 - 110} /{60 x 0.6 +1}= 10 mmol/LOne liter of this fluid would increase Na by 10 mmol/L. Dose of hypertonic saline at 200 mL/hr until symptoms improve. Maximum 1 litre of 3% NS should be given in 24 hour.
  • 41. Goal: Minimum correction of serum [Na] by 4-8 mmol/L per day, with a lower goal of 4-6 mmol/L per day if the risk of ODS is high. Limits not to exceed: • 8-10 mmol/L in any 24-hour period. Treatment of chronic hyponatremia(Avoiding ODS)
  • 42. 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.
  • 43. 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 - Demeclocycline 150- 300 mg PO tid or qid -Fludrocortisone 0.05-0.2 mg bid Treatment of euvolemic hyponatremia
  • 44. 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].
  • 45. HeartFailure- for patients with mild to moderate symptoms, begin with fluid restriction (1 L/d total) and, if signs of volume overload are present, administer loop diuretics. If the serum [Na] does not correct to the desired level, lift the fluid restriction and start either conivaptan or tolvaptan. Treatment of hypovolemic hyponatremia
  • 46. Cirrhosis-Severe daily fluid restriction, Vaptans an alternative choice if fluid restriction has failed to maintain a serum [Na] 130 mmol/L; however, tolvaptan use should be restricted to cases where the potential clinical benefit outweighs the risk of worsened liver function, such as in patients with end-stage liver disease and severe hyponatremia who are awaiting imminent liver transplantation.
  • 47. CKD-Restricting fluid intake. Aquaretics (vaptans) can be employed{not be expected to cause a clinically significant aquaresis with severe renal impairment (ie, serum creatinine >2.5 mg/dL)}.
  • 48. Role of VAPTANS Vaptans have long been anticipated as a more effective method to treat hyponatremia by virtue of their unique effect to selectively increase solute-free water excretion by the kidneys. Although not C/I with decreased renal function, these agents generally will not be effective if S.Cr is >2.5mg%.
  • 49. Conivaptan Tolvaptan Lixivaptan Receptor V1a/V2 antagonist V2 antagonist V2 antagonist Route i.v Oral Oral Urine volume ↑ ↑ ↑ Urine osmolality ↓ ↓ ↓ Sodium excretion/d ↔ ↔ ↔ at low dose, ↑at high dose Status FDA approved FDA & EMAapproved Phase 3 completed Dosage 20mg over 30min f/b cont inf 20-40mg/d 15mg on D1, then titrate to 30-60mg/d - Duration of treatment Max 4days (interaction with CYP3A4) ≤30days(risk of hepatic injury) - Side effects Headache, thirst, hypokalemia Drymouth, thirst, dizziness, hypotension - Indications Euvolumic and hypervolumic hyponatremia Euvolumic and hypervolumic hyponatremia -
  • 51. 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).
  • 52. • Patients can present para- or quadraparesis, dysphagia, dysarthria, diplopia, a "locked-in syndrome," and/or loss of consciousness. • Most commonly affected area is pons. • Other regions of the brain affected in ODS: (in order of frequency) cerebellum, lateral geniculate body, thalamus, putamen, and cerebral cortex or subcortex.
  • 53. • As these lesions may not appear until 2 weeks after development, a diagnosis of myelinolysis should not be excluded if the imaging is initially normal.
  • 54. Starting serum [Na] ≥120 mmol/L: Intervention unnecessary. Starting serum [Na] <120 mmol/L: Withhold the next dose of vaptan if the correction is >8 mmol/L; Consider therapeutic re-lowering of serum [Na] if correction exceeds therapeutic limits; Consider administration of high-dose glucocorticoids (eg, dexamethasone, 4 mg every 6 hrs) for 24-48hrs following the excessive correction. Managing excessive correction of chronic hyponatremia
  • 55. Re-lowering serum [Na]: Administer desmopressin to prevent further water losses: 2-4 mg every 8 hours parenterally; Replace water orally or as 5% dextrose in water intravenously: 3 mL/kg/h; Recheck serum [Na] hourly and continue therapy infusion until serum [Na] is reduced to goal
  • 56. Hypotonic hyponatremia/tru e hyponatremia Pseudohyponatremia/osmotic related Primary renal disease Impaired renal function Access volume status Access renal status Normal Volume depletion Edema – CHF, cirrhosis, nephrotic syndrome Ur, Na + <20 = diarrhoea, vomiting, burns, pancreatitis Ur, Na + >20 = diuretics, salt losing nephropathy Normal volume Adrenal & thyroid function Adrenal & thyroid insufficiency Normal Access Urine osmolality(Abl e to dilute urine) >100 mOsmol/kg Dilute urine Psychogenic polydipsia NO YES Access serum osmolality low Normal/high SIAD Approach to a case of hyponatremia
  • 57. Case Discussion  74-year-old man p/w recent gastroenteritis characterized by n/v/d x 5 days, in addition to fatigue and headache.  CT head (-) in ED. No focal neurologic deficits found. He looks dry on physical exam, with no evidence of fluid overload.  BMP significant for Na+ of 118, baseline unknown. Serum osmolality is 266. Urine osmolality is 377. Urine sodium is 8.  How would you approach this patient’s hyponatremia?  How would your approach be different if this patient presented with new-onset seizures?
  • 58. 74-year-old man p/w recent gastroenteritis characterized by n/v/d x 5 days, in addition to fatigue and headache. BMP significant for Na+ of 118, baseline unknown. Serum osmolality is 266. Urine osmolality is 377. How would you approach this patient’s hyponatremia? The steps: 1) Serum osmolality – 266, decreased (hypotonic) 2) Urine osmolality –377, increased (>100) 3) Volume status – hypovolemic 4) Urine Na, FeNa – urine Na 8, appropriately reabsorbing, likely volume depleted 2/2 N/V 5) Treatment: Mild symptoms, correct slowly w/ isotonic saline
  • 59. How would your approach be different if this patient presented with new-onset seizures? For symptomatic, severe hyponatremia, more rapid correction using 3% normal saline