Hyponatremia

causes and management of hyponatremia

1. Doha RasheedyAly

2. Hyponatremia
Definition
Epidemiology
Physiology
Pathophysiology
Types
Clinical Manifestations
Diagnosis
Treatment

3. Hyponatremia
•Definition:
–Commonly defined as a serum sodium concentration<
135 meq/L
–Hyponatremiarepresents a relative excess of water in
relation to sodium.
–occur due to:
1)Water retention dtimpaired free water excretion
2) Less: Na loss>water loss (thiazideinduced
hyponatremia)

4. Hyponatremia
Epidemiology:
Frequency
Hyponatremiais the most common electrolyte disorder
prevalence of approximately 7%
30% of patients treated in the intensive care unit
50% of NHR had atleastone episode of hyponatremia.
ocw.jhsph.edu

5. Hyponatremia
Epidemiology Cont.
Mortality/Morbidity
Acute hyponatremia(developing over 48 h or less) are subject
to more severe degrees of cerebral edema
sodium level is less than 105 mEq/L, the mortality is over 50%
Chronic hyponatremia(developing over more than 48 h)
experience milder degrees of cerebral edema
Brainstem herniationhas not been observed in patients with
chronic hyponatremia

6. Hyponatremia
Physiology
Serum sodium concentration regulation:
stimulation of thirst
secretion of ADH
feedback mechanisms of the renin-
angiotensin-aldosteronesystem
renal handling of filtered sodium
www.daviddarling.info

7. 1-Stimulation of thirst: Thirst center is located in the
anteriolateralcenter of the hypothalamus
Osmolalityincreases
Main driving force
Only requires an increase of 2% -3%
Blood volume or pressure is reduced
Requires a decrease of 10% -15%
2-Secretion of ADH
Synthesized by the neuroendocrinecells in the supraopticand
paraventricularnuclei of the hypothalamus
Triggers:
Osmolalityof body fluids
A change of about 1%
Volume and pressure of the vascular system
Increases the permeability of the collecting duct to water and urea

8. ADH
No ADH: ADH Present:

9. Renal Physiology

10. Age related changes of water metabolism:
The elderly have a delayed and less intense thirst response than
do younger person
total body water decreases because of an increase in fat and a
decrease in lean body mass (from about 60% of body weight in
healthy young adults to about 45% of body weight in the elderly
The ability to concentrate urine decreases with age in part
because of tubular senescence.
Many elderly persons also have resistance to the renal action of
ADH, ie, a form of acquired partial nephrogenicdiabetes
insipidus.
Decreased renal conservation of Na dt:
Nephronloss
Decreased reninand aldosterone
Increased ANP
An age-related decrease in serum sodium concentration of 1
mEq/L/decade occurs after age 40

11. hyponatremiaoccur when some condition impairs
normal free water excretion or Na loss exceed water loss
acute drop in the serum osmolality:
neuronal cell swelling occurs due to the water shift from the
extracellular space to the intracellular space
Swelling of the brain cells elicits 2 responses for
osmoregulation, as follows:
It inhibits ADH secretion and hypothalamic thirst center
immediate cellular adaptation
Pathophysiology

12. Clinical Manifestations
most patients with a serum sodium concentration
exceeding 125 mEq/L are asymptomatic
Patients with acutely developing hyponatremiaare
typically symptomatic at a level of approximately 120
mEq/L
Most abnormal findings on physical examination are
characteristically neurologic in origin
patients may exhibit signs of hypovolemiaor
hypervolemia

13. Manifestations
In acute hyponatremia, osmotic forces cause water
movement into brain cells leading to cerebral edema
Mild Sx: anorexia, nausea, lethargy
Mod Sx: disoriented, agitated, neurodeficit
SevSx: seizures, coma, death

14. Serum Osm: 275-290 mosm/kg
Calc = 2x[Na] + [glucose]/18 + [ BUN]/2.8 +
[ethanol]/4.6
Plasma osmolarity:

15. 1. Hypotonic hyponatremia
2.Hypertonichyponatremia:(Redistributive
hyponatremia)
excessofanothereffectiveosmole(glc,mannitol)thatdrawswater
intravenously.
hyperglycemia(1.6/100)
3.Isotonichyponatremia:
*Pseudohyponatremia;hyperlipidemiaorhyperprotienemiaresultsin
lowmeasuredNa⁺concentration(butosmolalityisnormal)
itisararelabartifact
*Artefactualhyponatremia;takingbloodfromadriparmintowhichalow
sodiumfluidisbeinginfused.
Classification According to Plasma Osmolality:

17. Step-wise Approach
Serum Osm: 275-290 mosm/kg
Calc = 2x[Na] + [glucose]/18 + [ BUN]/2.8 + [ethanol]/4.6
Isotonic: PseudohypoNa
Hyperproteinemia, Hyperlipidemia
High/Hyperosmolar
hyperglycemia (1.6/100), mannitol
Low/Hypoosmolar

19. Labs
Plasma Osm
Hyperosmolar, Isoosmolar, Hypoosmolar
Urine Osm
Are you able to excrete the extra H2O?
< or > 100 mosm/kg

21. Labs
Plasma Osm
Urine Osm
Volume Status
Effective circulating volume
XS TBW:TB Na
TB Na is reflected by ECF volume status

23. Volume Status
Euvolemic
H2O Inc & Na Stable
Hypervolemic
H2O Inc & Na Inc
H2O > Na
Hypovolemic
H2O Dec & Na Dec
H2O < Na

24. Volume Status
Hypovolemic
GI solute loss
diarrhea, emesis
Third-spacing
ileus, pancreatitis
Diuretic use
Addison disease
Salt-wasting nephritis
Hypervolemicw/decECV
DecompensatedCHF
Advanced liver cirrhosis
Renal Failure
Euvolemic
SIADH
Diuretic use
Glucocorticoiddeficiency
Hypothyroidism
Beer Potomania, psychogenic
polydipsia
Reset osmostat

25. SIADH:
downward resetting of the osmostat
Pulmonary Disease
Small cell, pneumonia, TB, sarcoidosis
Cerebral Diseases
CVA, Temporal arteritis, meningitis, encephalitis
Medications
SSRI, Antipsychotics, Opiates, Depakote, Tegratol
miscellaneous
pain, nausea, post op.)

26. Labs
Plasma Osm: 275-290 mosm/kg
Urine Osm
Volume Status
Urine Na Concentration

29. four issues must be addressed
Asymptomatic vs.symptomatic
acute (within 48 hours)
chronic (>48 hours)
Volume status
1
st
step is to calculate the total body water
total body water (TBW) = 0.6 ×body weight
Treatment

30. .
Treatment Cont
nextdecidewhatourdesiredcorrectionrateshouldbe
Symptomatic
immediateincreaseinserumNalevelby8to10meq/Lin4to
6hourswithhypertonicsalineisrecommended
acutehyponatremia
morerapidcorrectionmaybepossible
8to10meq/Lin4to8hours
chronichyponatremia
slowerratesofcorrection
12meq/Lin24hours

31. IV Fluids
One liter of Lactated Ringer's Solution contains:
130 mEqof sodium ion = 130 mmol/L
109 mEqof chloride ion = 109 mmol/L
28 mEqof lactate = 28 mmol/L
4 mEqof potassium ion = 4 mmol/L
3 mEqof calcium ion = 1.5 mmol/L
One liter of Normal Saline contains:
154 mEq/L of Na
+
and Cl
−
One liter of 3% saline contains:
514 mEq/L of Na
+
and Cl
−

32. ??????Na+deficit= Target Na -Current Na e.g. 120-115
Total body Na+ deficit= Na+deficitx total body water
= 5 x 0.6x body wt (50kgs)
= 125meq
??????Amount of 3% NaClneeded(Na=513meq/L)= 125/513=
240ml
??????Rate of infusion=0.5meq/hour=10 hours
=24ml/hour

33. SIADH
response to isotonic saline is different in the SIADH
In hypovolemiaboth the sodium and water are retained
sodium handling is intact in SIADH
administered sodium will be excreted in the urine, while some
of the water may be retained
possible worsening the hyponatremia

34. Water restriction
0.5-1 liter/day
Salt tablets
Demeclocycline
Inhibits the effects of ADH
Onset of action may require up to one week
SIADH

35. Volume depletion:
Isotonic saline:
raises plasma sodium by 1-2 meq/L for every liter of fluid infused
since saline has higher Na concentration (154 meq/L) than
hyponatremicplasma
volume repletion removes stimulation of ADH

36. CHF, Cirrhosis, Nephroticsyndrome
Patients have increased total body sodium stores.
Treatment consists of sodium and water restriction
and attention to the underlying cause.Thevasopressin
receptor antagonists conivaptan(Vaprisol) and
tolvaptan(Samsca) are now approved for use in
hospitalized patients with hypervolemic
hyponatremia, though clinical experience is scant

37. % NaCl3Indications for
Symptomatic hyponatremia(SZ, coma)
Acute severe hyponatremia(<24h, < 120
mEq/L)
SAH with hyponatremiaworsening on 0.9%
NaCl

38. Why don’t we correct the hyponatremia
rapidly??
It results in a severe neurological syndrome due to
local areas of demyelination called “Central
Pontine Myelinosis” or “Osmotic Demyelination
Syndrome”.
Symptoms include dysarthia, dysphagia, spastic
quadriplegia, psuedobulbar palsy, and respiratory
arrest.
Occurs in the ponsmostly, but also in the basal
ganglia, internal capsule, and cerebral cortex.