Hyponatremia

1. Hyponatremia Management
Dr. Fateh Akram
DTCD STUDENT
Medicine Unit VI
National Institute of Diseases of The Chest & Hospital

2. Sodium Water
Hyponatremia
“Hyper-acquemia”

3. Normal water balance
Normal water intake(1-1.5 L/d)
Intracellular Extracellular
Compartment compartment
28 L 14 L
42 L TBW
60% of body
weight
Fixed water excretion
Stool Sweat Lungs
0.1 L/d 0.1 L/d 0.3 L/d
Total insensible losses
0.5 L/d
Water
Of
Cellular
Metabol
0.3-0.5
L/d
Variable water excretion
Kidney
Total urine output
1-1.5 L/d
Water
intake
Water
excretion
ADH

4. Hyponatremia

5. Mechanism
of
Hyponatremia

6. Hyponatremia
Supervenes when
free water intake >> free water
excretion
Main defense
excretion of free water by kidneys

8. Identifying
types of
Hyponatremia

10. Hypotonic Hyponatremia

11. Hypotonic Hyponatremia
Hypovolemic Euvolemic Hypervolemic
Urine Na
<30 >30
ExtraRenal Renal
1.Diarrhea
2.Vomiting
3.Hemorrhage
4.Sweating
1.Diuretics
2.Mineralocorticoid def
3.Salt losing Nephropathies
4.Cerebral salt wasting 
1.SIADH 
2.Glucocorticoid def
3.Hypothyroidism
4.Poor solute intake 
-Tea Toast syndrome
- Beer potomania
5.Post op / Hospital acquired
1.CHF
2.Cirrhosis
3.Nephrotic synd
4.Advanced CRF

12. Hypotonic hyponatremia
(Vol status indeterminate)
Urine Na <30 :
Respond to 0.9 NS
Volume depleted
Urine Na > 30 :
No response to 0.9 NS
Likely to have SIADH

13. Euvolemic Hypotonic
Hyponatremia

14. SIADH
Criteria for diagnosis:
 P osm <275 mOsm/kg
 U osm >100 mOsm/kg
 Clinical euvolemia
 Urine Na > 30mmol/L while on normal salt intake
 Normal thyroid, adrenal and renal functions
 Inappropriately elevated AVP levels in 85-90%

15. Tumors small cell CA, Head & Neck
CNS Trauma, tumors, meningitis, CVA
Pulmonary Pneumonia, PTB, resp failure, asthma
Mechanical ventilation, COPD
Drugs DDAVP, Diabinese, NSAIDS, opiates,
Carbamazepine, SSRI, Tricyclic, Thiazides
Ecstasy, ACE-I, Omeprazole
Miscellaneous Pain, Nausea, surgery, stress,
Alcohol withdrawal
SIADH : Common Causes

16. SIADH : Treatment
 Discontinue offending agent
 Treatment of etiology (infection, pain)
 Fluid restriction (for Chronic asymptomatic
Hyponatremia)

17. Euvolemic Hypotonic hyponatremia
Poor solute Intake
Beer Potomania, Tea Toast syndrome
Urine Volume =
Normal Urinary Electrolytes Normal Urinary Urea
Na+ , K+ = 150 + 50 = 200 Catabolism= 75-100
Accompanying anions= 200 Diet ~50 mM/10 gm of dietary protein
Total 400 mM/day Total 400-500 mM/day
Urinary solute excretion
Urinary Osmolality
Clinical setting of low solute intake:
- Alcoholism (Beer Potomania)
- Anorexia (Tea and Toast Diet)
Urinary solute excretion
in person on normal diet-
800-900 mM/day

18. Euvolemic Hypotonic hyponatremia
Poor solute Intake
Treatment
1. Increase solute intake –
• High protein diet
• Salt tablets or high dietary salt
• Urea
2. Fluid restriction

20. Hospital acquired Hyponatremia
Virtually every hospitalized patient has
potential stimulus for AVP excess
Administration of hypotonic fluid with excess
AVP are at risk for Hyponatremia
Chung HM et al, Arch Inter Med 2002

21. Hospital acquired hyponatremia
• Ringer’s Lactate (Sodium 77) is hypotonic
and can produce hyponatremia
• No justification for Ringers lactate in post op
period
• Administration of 0.9 saline is safe
• No reports of 0.9 Saline causing neurological
complications of hyponatremiaSteele A et al, Ann Intern Med 1997
Moritz ML et al, J Am Soc Nephrol 2005

22. Clinical features
And
Brain Adaption

23. Hyponatremia Symptoms

25. Cerebral adaption to decrease
cerebral edema
Early 1-3 hrs
CSF distribution
Later (> 3 hrs)
Loss of Osmolytes and electrolytes:
 Glutamate, Inositol, Taurine,
 Urea, K, Na, Creatinine

26. Investigation
History & volume
status
Serum Osmolality
Urine Osmolality/sp gr
Urine Na
S Cr/urea/K
T3/T4/TSH
CXR
CT Scan Manisha Sahay

27. Treatment

28. Extensive data suggest that the serum sodium
should be raised by no more than 10 mEq/L over 24
hours. Correction by 6 mEq/L in 24 hours has been
dubbed the "rule of sixes."The rule of sixes is as
follows: "Six-a-day makes sense for safety. Six in 6
hours for severe symptoms and stop."

29. Acute Hyponatremia:
 Less than 48 hrs
 Neurologic symptoms due to brain edema
 Rapid correction well tolerated
Chronic Hyponatremia:
More than 48 hrs or unknown time
 Mild brain edema (<10%)
 Sensitive to Na correction rate
 Aim to increase Na by 10% (not more than 12 in 24
hrs)

30.  How long has hyponatremia been present?
 Does the patient have symptoms?
 Does the patient have risk factors for
development of neurologic complications?

31. Monitoring of patients
 Volume status
 Daily weight
 Frequent Serum Na, K
 Plasma Osmolality
 Urine Na, K, osmolality
 Strict Input and Output

32. Basic concept
 Free water intake << Free water output
AND
Na, K intake >> Na, K output
 Needed Info:
 Serum Na , osmolality
 Urine Na, K, Osmolality
 Strict Input/ Output
 Rate of correction

33. Hyponatremia
Chronic
AsymptomaticSymptomatic
Long term
management
Treat etiology
Water restriction
Demeclocycline
Some immediate correction
Hypertonic saline
+ Furosemide
Change to water restriction
Frequent serum & urine
electrolytes
Do not exceed 12 meq/l/d
Emergency
Hypertonic
saline+
furosemide
Acute <48 hrs Chronic>48 hrs
No immediate
Correction needed
Thurman et al,Therapy in nephrology and

34. Treatment of Symptomatic
Hyponatremia

35.  Treatment based on neurological symptoms and
not on Sodium
 Needs aggressive management with 3%NaCl
 No role of fluid restriction alone
 Treatment should precede any neuroimaging
 Treatment in monitored setting
 Sodium levels measured every 2 hours

36.  Impending herniation: Sz, resp arrest,, obtundation,
Decorticate posturing, dilated pupils:
 100 ml of 3% NaCl as a bolus over 10 min to rapidly
reverse brain edema.
 Repeat bolus as required till symptoms improve
 Encephalopathy: Headache, N/V, Altered mental status:
3% NaCl @ 50-100 ml/hr
 Calculating 3% saline rate:
Weight in kg x desired rate of increase in Serum Na

37.  Monitor [Na] every 2-4 hrs
 Stop active correction when appropriate end point is
reached:
 Patient becomes asymptomatic
 Safe Na levels reached (generally 120)
 Total correction 12 mmol in 24 hrs or 18-20 mmol
in 48 hrs
 Complete rest of correction with - fluid restriction

38.  Attend to underlying cause
 No immediate correction needed
 Fluid restriction
Urine Na + K
Plasma Na
Recommended water intake
>1 < 500 ml/day
-1 500 to 700 ml/day
< 1 < 1000 ml/day
D Ellison, T Berl. NEJM 2007;356:2064-72

39. Treatment Mechanism Dose Advantage Limitations
Fluid
restriction
Decreases
availability of free
water
Variable Effective
Inexpensive
Non compliance
Encourage dietary
salt and protein
Solutes required
for free water
excretion
Variable
Demeclocycline ↓ ADH response 300-600 mg BID Effective
Unrestricted
water intake
Nephrotoxic,
Polyuria,
Photosensitive
V-2 Receptor
antagonist -
Conivaptan
Antagonize ADH
receptor
20-40 mg/day
IV (Vaprisol)
Effective Available only as
IV

40. Complications of treatment
Acute Cerebral edema
Osmotic Demyelination

41. Take home message
Hyponatremia –a common, life threatening
problem
 In presence of ADH concentrated urine is formed
Treatment – Basic concept:
 Free water Input << Free water Output
 Na+K Input >> Na+K Output
Step wise evaluation important

42. Hyponatremia
AsymptomaticSymptomatic
Long term managementHypertonic
saline
Acute <48 hrs
No immediate
Correction needed
Emergency
Go slow