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1)Hypo-osmolality
↓ ECF b/c of excessive H2O loss & ↓ intake of
Na & H2O
2) If hypo-osmolality is corrected too rapidly that
is >12mEq/L/day pt may experience an acute ↓ BRAI
in brain cell vol which may further lead to N
demyelinating brain injury b/c ↓ in plasma INJU
tonicity results in movement of H2O into cells
until the osmolality of the cells equals that of
RY
ECF. Neurons have the capacity to adapt to ↑ in
cell vol by actively transporting K & other
osmotically active osmolytes such as taurine,
glutamine & innositol out of cell. H2O will
redistribute into tubular spaces until osmotic TO
O
RAP
ID
COR
1) Pseudohyponatremia
In both these cases pt show falsely
hyponatremia b/c of the elevated HYPO
Uosm
>450mosm/kg
Serum osmolarity ●
●
CHF
UNa
Cirrhosis< 20
Nephrosis
mEq/L
Edema
Uosm
>100mosm/kg
●
Exclude
●
UNa > 20
hypothyroidism
Hypocortism
●
● mEq/L
Renal failure
SIADH
Uosm
>100mosm/kg
●
Primary
UNa < 20
polydipsia
●
Low solute
mEq/L
intake
Uosm <
100mosm/kg
CLINICAL PRESENTATION
Pts with SNa values > 125mEq/L are generally asymptomatic
except when hyponatremia develops in < 24 hrs (0.5 mEq/L/h)
Nausea
↑ neuronal
●
●
↓ed skin turgor
↓ ECF
●
Malaise
●
Orthostatic
cell vol /
●
Headache
●
Seizures
hypotension
edema
Respiratory arrest
●
●
●
Dry mucus membranes
Cerebral edema
DESIRED OUTCOME/GOAL
• Symptomatic tx
• ↑ tonicity by infusing 3% hypertonic saline
TREATMENT OF HYPONATREMIA
OUTCOMES
• Restoration of BP to normal range
• Absence of orthostatic changes
• ↑ in CVP or PCP to > 10 cm H2O
• 0.9% NaCl infuse to correct vol deficit
2) TX OF HYPERVOLEMIC HYPOTONIC HYPONATREMIA
A) ASYMPTOMATIC
GOALS
1. Induce negative water balance by restricting water to
<1000-1200ml/day
2. Maintenance of SNa >125mEq/L
Tx
3. Should be txd with hypertonic saline
4. Digitalis
5. ACEIs/ARB
• ACEIs dose should be titrated to keep SBP to 110-130 mmHg
• If SrCr >30% → reduce dose or discontinue ACEIs
• AD EFFECT
a) Hyperkalemia
b) Decline in renal function
4. Loop diuretic
B) ACUTE SYMPTOMATIC HYPEVOLEMIC HYPOTONIC
HYPONATREMIA
• Give 3% NaCl
• SNa should be increased up to 120 mEq/L
• Infusion give @ rate of 1.5-2 mEq/L/h
• SNa conc should not exceed 12 mEq within first 24
hrs
3) ASYMPTOMATIC EUVOLEMIC HYPOTONIC
HYPONATREMIA
GOAL
EPIDEMIOLOGY/ETIOLOGY
• If H2O lossess because of any reason ECF vol ↓es but the Na is
more, neuronal cell start releasing H2O from ICF → ECF
• Cerebral adaptation mechanism (CAM) is the feature through
which neurons protect themselves against the vol changes to
prevent the damage by managing the Na in ECF
• There are certain osmolytes which are developed by neurons
within 24 hrs after hypernatremia develops. These osmolytes
start balancing the Na in the ECF & H2O moves back towards
ICF b/c of synthesized osmolytes thus restoring the neuronal
cell vol
PATHOPHYSIOLOGY
HYPOVOLEMIC HYPERNATREMIA
Loss of H2O + Na
(H2O loss > Na loss)
Gain of H2O + Na
RENAL
ADRENAL
GI
LUNGS
Loss of H2O
SKIN
GI
Na overload Skin loss
Iatragenic
Mineralocorticoid excess Osmotic diuresis
Primary polydipsia
ECF VOL
Uosm
Uosm
Uosm >
450mOsm/kg < 250mOsm/kg > 300mOsm/kg
> 300mOsm/kg
DI
Osmotic diuresis
(appropriate)
Response to
Postural hypotention desmopressin
Osmotic diuresis
(inappropriate) Yes No postobstructive Na excess
Yes No
Central DI
• Txd with intranasally desmopressin @ dose of 10μg OD
(BD in adults)
• b/c of variable absorption DI is txd with DDAVP each
insufflation of which delivers 10μg of desmopressin
acetate @ a conc of 100μg/ml
• Desmopressin dose shud b adjusted to prevent nocturia to
result in daily urine vol of 1.5-2 L & maintain Sna in the 137-
142mEq/L
• Sna conc shud b measured every 3-4 days during the initial
dose titration period then to 2-4 months
NEPHROGENIC DI
Induce ECFVD (1-1.5L) with thiazide diuretic & dietry Na
restriction (85mEq Na+ or 2000 mg NaCl per day) which can
decrease the Uvol by 50%. This effect is known as “Thiazide
paradoxical antidiuretc effect”