Hyponatremia is a common electrolyte disorder in diverse fields of medicine. A sound understanding of Physiology is essential for its management. Real life clinical examples are described
16. Osmoreg. Vs Vol.reg
• What is sensed?
• Plasma OSMOLALITY
• Sensor?
• OsmoR
• Effector?
• ADH and thirst
• Final say
• Water excretion /
retention
• What is sensed?
• Eff.Circ.BV
• Sensor?
• CAROTID BARO R,ATR.
• Renal AA
• Effector?
• RAAS,ANP,SS
• Final say
• Urine Na
excretion/Retention
17. In volume depletion states when
ADH is stimulated which takes
precedence ?
Water is retained more and serum sodium lowered
18.
19. Clinical approach to HypoNa
•1% of healthy population
•5-8 % of hospitalised patients
•30% of ICU patients
20. Is it serious ?
• Marker of severity of underlying disease
• CCF.
• Cirrhosis.
• Advanced cancer.
• Marker of increased mortality
• Treatment may be more deleterious in
some !
21. 4 essentials
1. History
2. Plasma osm.
3. Volume status
4. Urine Sodium
22.
23. Don’t jump to treatment!!
Avoid misdiagnosis !
• Sampling error ? Common
• Hyperlipidemia ? Use ISE ( Not Flame
Photometer)
• Multiple Myeloma ? Use ISE ( - do - )
• Hyperglycemia ? Every 100 mg increase in glucose
reduces serum Sodium by 1.6 - 2.4 mEq/L
• Drugs and chemicals? Glycine,Mannitol.
24. Hyperglycemia – Hyperosmolar
hyponatremia
Water
Glucose is osmotically
Active
Translocational
hyponatremia
Serum osmolality will be high
25.
26. LOOP D block both
conc.and dilution
THIAZIDES BLOCK DILUTION
ALONE
Urine Na and K moderate Urine Na and K very high
31. Therapeutic Strategy Based On
• 1. Volume Status of Patient
• 2. Presence of Absence of Symptoms
• 3. Duration of Hypoosmolality
• 4. Presence of absence of risk factors for
development of neurological complication
(Osmotic demyelination is rare in patients
with initial Na+ > 120mEq/L)
32. Clinical scenario 1
• 28 years old female
• Admitted for delivery
• Prolonged labour
• Had to be taken up for cesarian
• Post op coma
• Seizures
• Fluid orders – NS 3000 ml /24 hrs
• BP 100/80- Serum Sodium 110 mEq/L
33. Why hyponatremia
Source of free water
Was given Normal saline
3 Litres /24 hours
Free water intake due to anxiety
ADH is acting
Post op pain
Anxiety
Nausea due to
analgesics
DESALINATION syndrome
34. e- 300 mOsm x 3
900 Mosm
ADH
CONCENTRATES
URINE
600 Mosm /L = 1.5 L of urine
3 L of Saline
Thus 1.5 Litres of free water
is retained in body !
35. 1.5 L WATER
270 mOsm
270 mOsm
K 135 Na – 135
26 L 17 .5 L
1L
0.5L
36. Cerebral edema and Brain herniation
36
CNS ENCASED IN SKULL
Acute water excess
Neuronal edema
Tentorial herniation
Neurog.Pul.edema
38. Scenario 2
56 years old male
Alcoholic cirrhosis
Edema , Ascites
Oliguria
Sleepiness
S.Sodium 113/K 2.3
?Chronic hyponatremia – beware!
38
39.
40.
41. Chronic hyponatremia – Brain adapts to keep
the edema within limits
Aminoacids.Myoinositol
Rapid correction leads on to
cell shrinkage and Demyelination.
42. Calculation
• 60% of body weight is water
• 65 x 0.6 = 39 L
• 123-113 = 8
• 39x 8 = 312 Meq needed
• 1ml of 3% saline = 0.5 mEq of Na
• Sodium deficit = 624 ml
• 624 /24 hours = 26 ml/hr
• Serum Na measure q2-4 hrs
42
43. Adrogue’s Formula*
• Change in serum Sodium=
(Bottle Na+ + Bottle K+) - serum Na+
total body water + 1
• Easier to calculate
*Horacio J Adrogue, Nicholas E Madias: Hyponatremia; NEJM Vol 342, No 21
May 25 (2000)
44. Janinic and Verbalis formula
• Rate ml/Kg/Hr = Goal rate of rise
mmol/Kg/Hr
• 1ml/kg/hr = 1ml/kg/hr rise in Serum Na
• Ideal for those allergic to Math !!
45. Chronic hyponatremia
• Water restriction
• Demeclorcycline 300 -600 mg tid
• Lithium
• Oral urea
• VAPTANS
46. 19/9/2010
K
Na
moves into cell producing
hyponatremia
46
Tirunelveli API , TVMC Auditorium
47. 19/9/2010
Treat with Intravenous potassium
Replenish the IC deficit of Potassium .
Sodium automatically comes up
If not replaced , then there is danger of
osmotic demyelination.
47
Tirunelveli API , TVMC Auditorium
52. SALT -1 ,SALT-2 and SALTWATER
• Oral Tolvaptan increased the serum sodium
levels significantly and safely in CCF,SIAD and
Cirrhosis.
• NOT USED IN ACUTE SYMPTOMATIC
HYPONATREMIA
• 2 CONCERNS
• INCREASED THIRST
• OVERLY RAPID CORRECTION OCCURRED in 1.8%
• No ODM ENCOUNTERED
54. Why ODS is not a major threat
• Short acting
• Possible to reverse the effect
• Frequent Na monitoring in major clinical
trials
• No threat of hypok as with diuretic +
Hypertonic saline regimen
• FDA Warning- Liver toxicity on prolonged
use in Cirrhosis
56. SIADH v.s. Cerebral Salt Wasting
SIADH CSW
Serum Na ↓ ↓
ECFv Normal ↓
UNa ↑ ↑↑
UOSM ↑ ↑
Urine volume N or ↓ ↑
Serum urate ↓ N or ↓
Urine urate ↑ N or ↑
57. Some Interesting Issues not
discussed
• Reset Osmostat
• Beer Potomania
• Glycine in TURP
• Exertional hyponatremia
• Ecstacy and hyponatremia