approach to sodium metabolism

1. ANGAN KARMAKAR
(JUNIOR RESIDENT)
CHAIRPERSON: PROF. A.K. SAHA

3. Functions of sodium
 Sodium and its attendant anions (Cl- and HCO3-) account
for 90% to 95% of osmotic pressure in ECF
 Determine membrane potential and neuromuscular
excitability
 Influences acid-base balance
 Influences the activity of enzymes

4. Balance of sodium
 The content of sodium is 40~50 mmol /Kg of BW
 Sodium can be divided into two parts:
1)Exchangeable pool
60% of sodium is exchangeable
in ECF (50%) and in ICF(10%)
2)Non-exchangeable pool
40% of Na+ is bound to polyanionic proteoglycans in
bone ,cartilage,skin

6. NORMAL SODIUM METABOLISM
Sodium absorption
Via two mechanisms
1.freely permeable across the interstitial cell
2. symport with glucose and aminoacids

7. Sodium excretion
 Major determinant of balance
 Kidneys : extremely efficient
eliminates more if the intake of sodium is more and vice-
versa
does not eliminate sodium if there is no intake
 Gastrointestinal tract : second way
≤10% of the sodium intake is lost in feces

8. Sodium handling by kidney
 Absorbed at 3 main regions in the nephron
1.PCT– 2/3 of Na+ reabsorbed
2.TALH– 25-30% is reabsorbed via apical Na+ K+ 2Cl-
transporter
3.DCT– 5% by thiazide sensitive Na+ Cl- cotransporter
Finally Na+ reabsorption also occurs in cortical and
medullary collecting ducts via ENaC

9. Regulation of water and sodium
metabolism
 Thirst neural regulation
 Antidiuretic hormone
hormonal
 Aldosterone regulation
 Atrial natriuretic peptide

10. no thirst
increase of ECF
osmolality (1~2%)
hypovolemia
elevated
angiotensin II
dryness of
mouth
osmoreceptor
(anterior
hypothalamus)
volume receptor
in venae cavae and
atrium
thirst center (anterior hypothalamus)
sense of thirst and drink of water
decrease of ECF
osmolality
increase of
ECF volume
decrease of
angiotensin
concentration II
dryness disappears
Is it enough?
THIRST

11.  Thirst only is not enough to regulate the balance
of water and sodium
 The defects of (neuro-regulation) thirst are:
1)no obvious thirst in hypovolemia if osmolality is
not increased
2)in coma- no sense of thirst
3) too young baby, too old man

12. Antidiuretic hormone
 synthesis- hypothalamus
 storage & release-
Posterior pituitary
major regulator for water
output and reabsorption
in kidney

13. increase of ECF osmolality
(1~2%) via osmoreceptor
hypovolemia via volume
receptor
reduction of BP via
baroreceptors
synthesis
and release
of ADH
drugs (stimulate), alcohol
(inhibit)
Stress,Pain
Nausea
elevated angiotensin II
+
+
+
+
+

15. ALDOSTERONE
 Major regulator of sodium excretion and
reabsorption.
 steroid hormone produced by the adrenal cortex
 Factors stimulating aldosterone secretion:
1) Angiotensin II - major stimulator
2) decrease of sodium level in ECF
3) increase of potassium level in ECF

16. ATRIAL NATRIURETIC PEPTIDE
• released from atrium in response to increased atrial
stretch via mechanoreceptors
• Effects:
1.dilates renal blood vessels increase GFR
2.inhibits reabsorption of Na+ from collecting ducts
3.inhibit release of renin, aldosterone and ADH
4.endogenous antagonist to angiotensin II
• increases excretion of both water and sodium

17. Homeostasis

18. ECF
NORMAL
PERIPHERAL
PERFUSION
NORMAL
PERFUSION
PRESSURES
Normal Albumen
Normal plasma oncotic pressure
NORMAL
CARDIAC
OUTPUT
Normal Sodium
Normal tonicity
Holds the fluid volume in circulation
Holds the fluid volume in ECF
NORMAL
PATIENT
APPROACH TO SODIUM IMBALANCE

19. ECF
NORMAL
PERIPHERAL
PERFUSION
NORMAL
PERFUSION
PRESSURES
NORMAL
CARDIAC
OUTPUT
True hyponatremia
represents an increase
in free water relative to
sodium in the
extracellular fluids
HYPONATREMIA

20. ECF
NORMAL
PERIPHERAL
PERFUSION
NORMAL
PERFUSION
PRESSURES
NORMAL
CARDIAC
OUTPUT
True hyponatremia
represents an increase
in free water relative to
sodium in the
extracellular fluids
HYPONATREMIA

21. ECF
NORMAL
PERIPHERAL
PERFUSION
NORMAL
PERFUSION
PRESSURES
NORMAL
CARDIAC
OUTPUT
RESULTS FROM LOSS OF
WATER AND SODIUM
AND REPLACEMENT
WITH PURE WATER
HYPONATREMIA

22. ECF
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
Hyponatremia
CLINICAL
PICTURE
Hypovolemic

23. ECF
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
Hyponatremia
CLINICAL
PICTURE
Hypovolemic
CEREBRAL EDEMA
• INCREASED ICP
• SEIZURES
• ARDS
• RESPIRATORY ARREST

24. ECF
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
Hyponatremia
CLINICAL
PICTURE
Hypovolemic
CEREBRAL EDEMA
• INCREASED ICP
• SEIZURES
• ARDS
• RESPIRATORY ARREST
MANAGEMENT
• MANAGE THE VOLUME
STATUS
• REPLACE THE SODIUM
DEFICIT

25. ECF
Hyponatremia
CLINICAL
PICTURE
Hypovolemic
CEREBRAL EDEMA
• INCREASED ICP
• SEIZURES
• ARDS
• RESPIRATORY ARREST
SODIUM DEFICIT CALCULATION
NORMAL TBW X (130 – CURRENT Na)
MANAGEMENT
• MANAGE THE VOLUME
STATUS
• REPLACE THE SODIUM
DEFICIT

26. ECF
Hyponatremia
CLINICAL
PICTURE
Hypovolemic
CEREBRAL EDEMA
• INCREASED ICP
• SEIZURES
• ARDS
• RESPIRATORY ARREST
SODIUM DEFICIT CALCULATION
NORMAL TBW X (130 – CURRENT Na)
CAN BE REPLACED WITH
• 3% SODIUM CHLORIDE (513 mmol/litre)
• ISOTONIC SALINE (308 mmol/litre)
MANAGEMENT
• MANAGE THE VOLUME
STATUS
• REPLACE THE SODIUM
DEFICIT

27. Approach to hyponatremia

28. Hyponatremia- Diagnostic Approach
The concentration of
sodium in a
random (spot)
urine sample and its
osmolality shows
the sodium loss is
renal or extra-renal
in origin.

29. MANAGEMENT
Hyponatremia- Diagnostic Approach
HYPOVOLEMIC HYPONATREMIA
• Hypertonic saline (3% NaCl)
in symptomatic patients
• Isotonic saline in
asymptomatic patients
Important : Never increase the Na levels by > 0.5 mmol/L per hour
The concentration of
sodium in a
random (spot)
urine sample and its
osmolality shows
the sodium loss is
renal or extra-renal
in origin.

30. Hyponatremia- Diagnostic Approach
NORMOVOLEMIC HYPONATREMIA
• FLUID RESTRICTION
• Furosemide diuresis, combined with
• Hypertonic saline (3% NaCl)
in symptomatic patients
• VAPTANS
MANAGEMENT
The concentration of
sodium in a
random (spot)
urine sample and its
osmolality shows
the sodium loss is
renal or extra-renal
in origin.
Important : Never increase the Na levels by > 0.5 mmol/L per hour

31. SIADH…a diagnosis of exclusion
Bartter et al. American Journal of Medicine 1957

32. Hyponatremia- Diagnostic Approach
HYPERVOLEMIC HYPONATREMIA
• FLUID RESTRICTION
• Furosemide diuresis, in
asymptomatic patients
• Furosemide diuresis, with
judicious use of hypertonic saline
in symptomatic patients
MANAGEMENT
The concentration of
sodium in a
random (spot)
urine sample and its
osmolality shows
the sodium loss is
renal or extra-renal
in origin.
Important : Never increase the Na levels by > 0.5 mmol/L per hour

34. ECF
Loss of Hypotonic fluidNORMAL
PERIPHERAL
PERFUSION
NORMAL
PERFUSION
PRESSURES
NORMAL
CARDIAC
OUTPUT
CLINICAL
SCENARIO

35. ECF
Loss of Hypotonic fluidNORMAL
PERIPHERAL
PERFUSION
NORMAL
PERFUSION
PRESSURES
NORMAL
CARDIAC
OUTPUT
CLINICAL
SCENARIO
•Vomiting
•Diarrhoea
•Profuse diuresis

36. ECF
Loss of Hypotonic fluid
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
CLINICAL
SCENARIO
•Vomiting
•Diarrhoea
•Profuse diuresis

37. ECF
Loss of Hypotonic fluid
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
CLINICAL
SCENARIO
•Vomiting
•Diarrhoea
•Profuse diuresis
Eg: Serum sodium
> 165 mmol/L
Hypovolemic Hypernatremia

38. ECF
Loss of Hypotonic fluid
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
CLINICAL
SCENARIO
•Vomiting
•Diarrhoea
•Profuse diuresis
Brain cell shrinkage
Eg: Serum sodium
> 155 mmol/L
ENCEPHALOPATHY
• depressed consciousness
• frank coma
• generalized seizures
• focal neurological deficits
up to 50% mortality
Hypovolemic Hypernatremia

39. ECF
Loss of Hypotonic fluid
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
CLINICAL
SCENARIO
•Vomiting
•Diarrhoea
•Profuse diuresis
Brain cell shrinkage
Eg: Serum sodium
> 155 mmol/L
ENCEPHALOPATHY
• depressed consciousness
• frank coma
• generalized seizures
• focal neurological deficits
Brain cells
behave like
osmometers !
Hypovolemic Hypernatremia

40. ECF
Loss of Hypotonic fluid
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
CLINICAL
SCENARIO
•Vomiting
•Diarrhoea
•Profuse diuresis
Brain cell shrinkage
Eg: Serum sodium
> 155 mmol/L
Idio-osmoles
Partially restored
Partially restored
Partially restored
Hypovolemic Hypernatremia

41. ECF
Loss of Hypotonic fluid
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
CLINICAL
SCENARIO
•Vomiting
•Diarrhoea
•Profuse diuresis
Brain cell size restored
Eg: Serum sodium
> 155 mmol/L
Idio-osmoles
Partially restored
Partially restored
Partially restored
Hypovolemic Hypernatremia

42. ECF
Loss of Hypotonic fluid
PERIPHERAL
PERFUSION
PERFUSION
PRESSURES
CARDIAC
OUTPUT
CLINICAL
SCENARIO
•Vomiting
•Diarrhoea
•Profuse diuresis
Brain cell size restored
Eg: Serum sodium
> 155 mmol/L
Idio-osmoles
Partially restored
Partially restored
Partially restored
Management
…to restore the
perfusion status and
sodium deficit quickly…
…and to replace the
free water deficit
slowly (to prevent
intracellular
overhydration).
Hypovolemic Hypernatremia

43. ECF
Management
… to replace the
free water deficit
slowly (to prevent
intracellular
overhydration).
FREE WATER DEFICIT= {(PLASMA Na-140)/140}*TBW
Estimating the water deficit

44. Approach to hypernatremia

45. Treatment of hypernatremia

46. why only in brain cells?

47. Consequences of rapid change of
plasma sodium concentration

48. TAKE HOME MESSAGES…
 Do not just be carried away by Na levels
 Asses the patient clinically
 Asses volume status
 Correct intravascular volume first
 Correct deficit or excess slowly unless symptomatic
 Recheck response clinically & by lab tests

49. THANK YOU FOR LISTENING