This document discusses sodium imbalance and hyponatremia. It provides details on: - Normal sodium regulation and the causes of hyponatremia being related to water excess relative to sodium. - The approach to evaluating hyponatremia by measuring osmolality, estimating volume status, and getting urinary sodium and osmolality levels. - Specific causes of hyponatremia like SIADH, cerebral salt wasting, and mineralocorticoid deficiency. - The treatment of hyponatremia depending on if it is acute or chronic and correcting it slowly to avoid osmotic demyelination syndrome.

1. SODIUM IMBALANCE
By: Ram Gopal Maurya

2. SODIUM REGULATION
• Normal value: 135-145mEq/L.
• 85-90% sodium is extracellular.
• Sodium is responsible for more than 90%of total osmolality of
ECF.
• Major function is to maintain ECF volume and therefore
maintain blood pressure.
• Daily requirement is about 100mEq or 6gm of sodium
chloride.
• Excess salt is excreted chiefly by kidneys.
• Total body sodium is mainly regulated by aldosterone and
ANP.
• ADH, which is secreted in response to increased osmolality or
decreased blood pressure, primarily regulates [Na+]

3. HYPONATREMIA
• Plasma Na+ concentration <135 mM
• The concentration of sodium in ECF is a reflection
of the tonicity of body fluids, not of total body
sodium content.
• Hyponatremia can be associated with low, normal
or high tonicity.
• Hyponatremia-Most common abnormality
• 15-30% of hospitalized pnts.
• Basically a water imbalance.

4. Development of Hyponatremia
• Hyponatremia is a condition of water excess
relative to Na+.
• A defect in renal water excretion in the presence
of normal water intake is a prerequisite for the
development of hyponatremia.
• This defect in water excretion is due to high
circulating levels of antidiuretic hormone (ADH).
• With retention of water, hyponatremic patients
are unable to lower their urine osmolality < 100
mOsm/kg H2O with the exception of those with
psychogenic polydipsia and reset osmostat.

5. Approach to the Patient with
Hyponatremia
• Step 1: Measure Serum Osmolality.
plasma osmolality
normal low high
280-295 <280 >295
isosmolality hyposmolality hyperosmolality
Hyperproteinemia Hyperglycemia
Mannitol, Glycerol, Glycine
Hyperlipidemia

6. Step 2. Estimate volume status
volume status
Hypovolemic hypervolemic normovolemic
Renal causes Extrarenal causes
• Diuretics vomiting
diarrhoea
• Mineralocorticoid deficiency
• Salt-losing nephropathy
• Cerebral salt wasting

7. Hypervolemic hyponatremia
1. CHF
2. Cirrhosis
3. Nephrotic syndrome
4. AKI & CKD
Normovolemiv hyponatremia
1. Psychogenic polydipsia
2. Hypothyroidism
3. Glucocorticoid deficiency
4. Hypokalemia
5. Drugs: NSIAD
6. SIADH

8. Step 3: get urinary sodium and osmolality
done
1. Hypovolemic hyponatremia
UNa >20 mEq/L RENAL SODIUM LOSS
UNa <20 mEq/L EXTRARENAL SODIUM LOSS
2. Hypervolemic hypernatremia
UNa >20 mEq/L RENAL FAILURE
UNa <20 mEq/L CHF OR CHIRROSIS
3. Normovolemic hyponatremia
Uosm > 100 mosm/kg H2O EXCESS OF WATER INTAKE
Uosm < 100 mosm/kg H2O EXCESS WATER RETENTION

9. Syndrome Of Inappropriate ADH
(SIADH)
• 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%).

10. Diagnostic Criteria for SIADH
• plasma sodium concentration <135 mmol/l.
• plasma osmolality <280 mOsmol/kg.
• urine osmolality > 100 mOsmol/kg.
• urinary sodium concentration >20mEq/L.
• patient clinically euvolaemic.
• absence of clinical or biochemical features of
adrenal and thyroid dysfunction.

11. 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

12. Cerebral salt wasting
• 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.

13. parameter CSW SIADH
HYPOTONIA yes Yes
VOLUME STATUS Low Normal to high
CVP Low normal
HEMATOCRIT High Normal
BUN High low
URINE Na High High
Urine osmolality High High
Urine volume High Low
Plasma ADH Normal to high High
Brain natriuretic peptide Normal to high normal
treatment Salt, fludrocortisone Water restriction, 3 %
saline, loop diuretics,
demeclocycline, urea,
vaptans

14. Mineralocorticoid deficiency
• Hyperkalemia
• Hyponatremia
• hypotensive and/or hypovolemic patient with
• high urine Na+ concentration (much >20 mM)

15. Clinical diagnosis
• The symptoms primarily neurologic
• Development of cerebral edema within a rigid skull.
headache, lethargy, confusion, gait disorder, nausea,
vomiting .
• In severe hyponatremia as seizures, coma, brain-stem
herniation, permanent brain damage or death.
• Hypo-natremia
Mild <135
moderate <130
sever <120

16. Treatment of Hyponatremia
• as acute (< 48 h duration) or chronic (> 48 h
duration)
• Treatment of Acute Symptomatic Hyponatremia
medical emergency.
3 % NaCl is the fluid of choice, because it has high
osmolality than most of the patients’ urine
osmolality.
Raise serum Na+ 1–2 mEq/h for 3 h to 6 hrs from
baseline and maximum total 8-12 meq/l/day.

17. • amount of Na+ required to achieve the
desired level:
Amount of Na needed = total body water *
desired Na – actual Na.
• 1 L of 3 % NaCl contains 513 mEq of Na+
• One liter of NS contains: 154 mmol/L of Na+

18. • Equations : 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 + K)]-serum Na = [Na+] change by 1 liter of
infusate.
(total body water +1)

19. Treatment of Chronic Symptomatic
Hyponatremia
• For chronic hyponatremia, the plasma [Na]
should not rise faster than 0.5 mEq/L per hour
i.e. 10–12 mEq/L in 24 hours, and < 18 mEq in
48 hrs.
• Use 3 % NaCl, but Once symptoms and signs
improve, either water restriction or normal
saline should be started

20. Treatment of Asymptomatic
Hyponatremia
• In such patients, check volume status. For
hypovolemic patients, administration of
normal saline will improve both
hemodynamics and serum [Na+].
• FLUID EXCESS IS PRESENT.

21. • Fluid restriction required: the sum of urine
[Na+] and [K+] divided by serum [Na+] can be
used in the restriction of fluids/day.
Ratio Daily fluid intake (mL)
>1 <500
1 500 to 700
< 1 1000
simplest way to restrict fluids: input = output

22. Specific tratment
• SIADH:
1. Treat the underlying cause of SIADH
2. Restrict fluid.
3. DIURETICS : Furosemide (40 mg) can be tried with
high Na+ intake.
4. Demeclocycline at 300– 600 mg twice daily induces
nephrogenic diabetes insipidus. major problem with
demeclocycline is nephrotoxicity.
5. Osmotic diuresis
6. V2 receptor antagonists (vaptans) can be used to
suppress ADH action.

23. Osmotic Demyelination Syndrome
• Previously called central pontine myelinolysis, is a
complication of treatment of hyponatremia.
• Due to rapid correction of chronic hyponatremia.
• When serum [Na+] is rapidly raised, the plasma
osmolality becomes hypertonic to the brain with
resultant water movement from the brain. This
cerebral dehydration probably causes
myelinolysis and ODS.

24. • Several risk factors for precipitation of OSD have
been identified. These are:
• 1. Chronic
• 2. Serum [Na+] < 105 mEq/L
• 3. Chronic alcoholism
• 4. Malnutrition
• 5. Hypokalemia
• 6. Severe liver disease
• 7. Elderly women on thiazide diuretics

25. • Clinical Manifestations
• 1. Paraparesis or quadriparesis
• 2. Pseudobulbar symptoms (dysarthria or
dysphagia)
• 3. Locked-in syndrome (preserved intellectual
capacity without expression),
• 4. Movement or behavioral disorders
• Management is supportive.
• Early reports showed 100 % mortality.

26. HYPERNATREMIA
• Hypernatremia is defined as serum or plasma
[Na+] > 145 mEq/L
• Hypernatremia is seen in about 1% of
hospitalized patients and is more common
(7%) in intensive care unit patients.

27. Etiology
• Hypernatremia may be caused by a primary
Na gain or a water deficit, the latter being
much more common.
• Normally, this hyperosmolar state stimulates
thirst and the excretion of a maximally
concentrated urine. For hypernatremia to
persist, one or both of these compensatory
mechanisms must also be impaired.

28. Patients at Risk for Hypernatremia
1.Elderly
2. Children
3. Diabetics with uncontrolled glucose
4. Patients with polyuria
5. Hospitalized patients
a. Lack of adequate free water intake or administration.
b. Impaired water conservation due to concentrating inability
c. Lactulose administration
d. Osmotic diuretics (mannitol)
e. Normal or hypertonic saline administration
f. Tube feedings
g. Mechanical ventilation

29. Approach

30. Step 1: Estimate Volume Status
HYPO; NORMO; HYPER
Step 2: measure
1.Plasma and urine osmolalities
2. Urine Na+ and K+

32. Signs and Symptoms of Hypernatremia
• Mostly neurologic due to brain shrinkage and
tearing of cerebral vessels .
• Acute hypernatremia: nausea, vomiting, lethargy,
irritability, and weakness. These signs and
symptoms may progress to seizures and coma.
• Chronic hypernatremia (present for > 1–2 days):
less neurologic signs and symptoms because of
brain adaptation; however, weakness, nystagmus,
and depressed sensorium may be seen.

33. Specific Causes of Hypernatremia
• Central Diabetes insipidus (DI)
1. Central DI is due to failure to synthesize or release
ADH from hypothalamus.
2. Two types of central DI: complete and partial
3. Thirst mechanism is intact in most except in patients
with craniopharyngiomas (post-operative)
4. Urine osmolality is usually ≤ 100 mOsm/kg H2O in
complete form
5. Distal nephron responds to ADH action.
6. nocturia is common .
7. Post-traumatic, post-surgical, metastatic tumors,
granulomas, and CNS infections are the most
common causes of acquired central DI.

34. Nephrogenic DI
• Tubular resistance to ADH action despite
adequate circulating levels of ADH.
• Thirst mechanism is intact
• Urine osmolality is < 300 mOsm/kg H2O
• Causes are both congenital and acquired
• Acquired nephrogenic DI: Important causes
include CKD, hypokalemia, hypercalcemia,
protein malnutrition, sickle cell disease, and
lithium, or demeclocycline treatment.

35. • Gestational DI
• Occurs during late pregnancy and resolves
after delivery.
• Caused by degradation of vasopressin (ADH)
by the enzyme vasopressinase, and this
enzyme is produced by the placenta
• Treatment is desmopressin (dDAVP), which is
not degraded by vasopressinase.

36. APPORACH TO POLUURIA

37. TREATMENT OF HYPOVOLEMIC
HYPERNATREMIA
• Management is aimed at the two
consequences of hypotonic fluid loss: (a) loss
of sodium, (b) loss of water in excess of
sodium (the free water deficit).
• Volume Resuscitation:
any signs of a low flow state (e.g., cold
extremities, a decrease in blood pressure or
urine output) should prompt immediate
volume resuscitation with isotonic saline.

38. • Free Water Replacement: The calculation of
free water deficit
• Current TBW = Normal TBW × (140/Current
[PNa])
• H2O Deficit (L) = Normal TBW – Current TBW
= TBW ( 1 – 140/ Current NA)

39. • REPLACEMENT VOLUME: Free water deficits
are corrected with sodium-containing fluids
such as 0.45% NaCL
• Volume (L) = H2O Deficit × (140/[Na] in IV
Fluid)

40. • RATE OF REPLA CEMENT:
1. aggressive replacement of free water deficits
can produce cell swelling and cerebral edema.
2. the decrease in plasma [Na+] should not exceed
0.5 mEq/L per hour during free water
replacement
3. time needed to reduce the plasma [Na+] to 140
mEq/L at a rate of 0.5 mEq/L/hr is
Actual Na – 140
0.5

41. Treatment of normovolemic
hypernatremia
• Diabetes Insipidus:
1. The hallmark of DI is a dilute urine in the face
of hypertonic plasma.

43. • CENTAL DI
a. dDAVP is the drug of choice for central DI
b. Available as nasal spray or oral form
c. Use the lowest dose 5–10 µg nasally or 0.1 or
0.2 mg orally at bedtime to avoid nocturia
and hyponatremia.
d. VASOPRESSIN: dose is 2 to 5 Units of aqueous
vasopressin given subcutaneously every 4 to 6
hours

44. • NEPHROGENIC DI
• Congenital DI patients should receive enough
water to prevent dehydration.
• Thiazide diuretics may be helpful.
• Removal of the cause

45. • THANK YOU