DISORDERS OF SODIUM

• 1/3 ECF comprises of NA & accompanying anions, Cl &

HCO3 made 90% of total osmolality
•2/3 ICF comprises of K & accompanying anions (organic &
inorganic PO4)
• Differential conc of ICF & ECF is maintained by Na/K ATPase
pump
• Symptoms in pts with hyponatremia & hypernatremia is
related to alteration in cell vol
• Sosm is tightly regulated by kidneys & remains constant
(275-290mosm/kg) variate only 2-3%
Sosm=(2xSNa) + (Bglu/18) + (BUN/2.8)
SNa= Serum Na conc in mEq/L
Bglu= Glucose conc in mg/dl
BUN= Blood Urea Nitrogen in mg/dl
 ADH release by 2 mechanisms

 When plasma osmolality rises 1-2% or more ADH release

from posterior pituitary → binds with V2 rcs on basolateral
surface of renal tubular epithelial cells → activate 2nd msgr
rxn → H2O channel ( aquaporin 2) inserted in luminal cells
→ H2O possess from cell to peritubular capillaries → H2O
reabsorbs into circulation
↑ Sosm → ADH release +thirst stimulate

 EABV ↓es 5-10% → stimulate baroreceptors in chest &

neck → activate RAS → synthesis of Angio II → stimulate
both nonosmotic ADH release + thirst
 Hyponatremia
EPIDEMIOLOGY/ETIOLOGY
Abnormality in hospitalized pts
H
YP
O-
O
S
M
OL

REASONS FOR BRAIN INJURY: AL

IT
Y

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

equilibrium is achieved ↓ed brain H2O & edema

REC
TIO
N
OF
HYP
O-
OS
MO
LAR
ITY
REASON OF HYPONATREMIA

1. ↑ H2O & ↓ Na → b/c of impaired H2O excretion

2. H2O retention → b/c of nonosmotic ADH release
Causes
a) Hypovolemia
b) ↓ EABV in CHF pt
c) Nephrosis
d) Cirrhosis
e) SIADH
 PATHOPHISIOLOGY

1) Pseudohyponatremia
In both these cases pt show falsely
hyponatremia b/c of the elevated HYPO

plasma protein & lipids → total NATR

EMIA

blood vol ↑es & conc of Na falsely

comes low
2) Hypertonic hyponatremia
If osm ↑es by 15moSm/kg then pt having
tendency of developing hypertonic
hyponatremia Hyper-
proten
Hyper
liped
emia
• Hyper emia
In diebetic pt ↑Bglu b/c glucose is Glyci Man
-
contributing osmole glyce ne nitol
• During surgery if pt receiving glucine mia
for irrigation then glycine can absorb
in blood &→↑SoSm b/c glycine is
active osmole
• If pt receiving diuretic like mannitol
→ hypertonic hyponatremia b/c
mannitol absorb in blood
 ●
●
Renal losses
Extrarenal losses
● UNa >< 20
Diuretics
GI
●
●
Skin
Adrenal
● mEq/L
Lung
insufficiency

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

Avoid a rise in the SNa conc > 12 mEq/L in 24 hrs

Hypovolemic hypotonic hyponatremia

• Correct ECF by infusing 0.45% or 0.9% normal saline

• Restoration of organ perfusion

Hypervolemic & euvolemic hyponatremia

• Symptomatic tx
• ↑ tonicity by infusing 3% hypertonic saline
 TREATMENT OF HYPONATREMIA

1) TX HYPOVOLEMIC HYPOTONIC HYPONATREMIA

• Should be txed with normal saline (0.9%)

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

• Initial tx of HYPOTONICITY in pts with coma &

seizures

• 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

1. Induce negative water balance by restricting

water to 1000-1200ml/day
2. Correction of underlying cause
3. Drugs that could be contributing should be
identified & discontinues when possible
4. Maintenance of SNa >125mEq/L
Tx

1) Give 3% saline (513mEq/L)

2) Pts with SIADH may be txd by ↑ing solute intake with either
urea or NaCl &/or loop diuretics (furosemide) If Uosm >
300mosm/kg, initially at a dose of 40mg every 6 hrs
3) Demeclocycline initially 900-1200mg/day then ↓ed to 600-
900 mg/daytotal daily dose given in 3-4 divided doses
• (no role in acute management of severe
hyponatremia b/c of delayed onset of axn (3-6days))
• It is contraindicated in pts with liver disease &
cirrhosis, who are at high risk for demeclocycline
induced renal tubular toxicity & acute renal failure
4) Investigational ADH rcs antagonists
 HYPERNATREMIA

EPIDEMIOLOGY/ETIOLOGY

• Hypernatremia (SNa > 135mEq/l) is always associated with

hypertonicity
• Most commonly observed in pts with impaired thirst response,
infants, ventillator pt who are fibrile, geriatric pt, commatose
pt, sensorial losses
Symptoms of hypernatremia
• Postural hypotension
• Weakness
• Restlessness
• Confusion
• Coma
• Hemmorhage
 Symptoms appears b/c of ↓ neuronal cell vol when Sna >
160mEq/L

CEREBRAL ADAPTATION MECHANISM

• 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

HYPERVOLEMIC HYPERNATREMIA ISOVOLEMIC HYPERNATREMIA

Loss of H2O + Na
(H2O loss > Na loss)

Gain of H2O + Na
RENAL
ADRENAL
GI
LUNGS

Loss of H2O
SKIN

(Na gain > H2O gain)

GI
Na overload Skin loss
Iatragenic
Mineralocorticoid excess Osmotic diuresis
Primary polydipsia
 ECF VOL

LOW Normal or ↑ed

Uvol > 3L/day

Uvol < 3L/day Uvol > 3L/day

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

Nephrogenic D5W 1.5-

Control DI 2ml/kg/h
DI
H2O & Na Primaily H2O
depletion depletion
Loop diuretic
Desmopressin Thiazide +D5W
D5W diuretic
0.9% saline
TX OF HYPOVELEMIC HYPERNATREMIA

• Hypovolemic hypernatremia should initially b treated with

0.9% normal saline until hemodynamic stability is restored
• Initial infusion rate is 200-300ml/h
• intravascular vol is restored 0.45% saline or D5W can then b
infuse to correct water deficit
• Hypernatremia dvlops over few hrs may b corrected @
1mEq/L/h or 0.5mEq/L/h if dvlop more slowly
• Tx of hyperglycemia induce osmotic diuresis consist of
correcting the hyperglycemia with insulin + 0.9% normal saline
until signs of ECF depletion resolve (then same as above)
• The corrected Na lvl shud b adding 1.7mEq/L for every
100mg/dl rise in Sglu
TX OF HYPERVELEMIC HYPERNATREMIA

• Hypernatremia in pts with postobs diuresis shud b txd with

0.45% saline @ 1.5ml/kg/h
Males who are suffering from benign prostate hyperplasia &
prostrate cancer → bladder obstruction → formation of
urine but outlet obstruction → GFR ↓es → retention of
H2O & solutes but Na retention is more → leading to
hypervolemic hypernatremia

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”

(CONSIDER TABLE 51-3 )

SODIUM OVERLOAD

• Administer loop (frusemide 20-40mg every 6hrs) to facilitate

excreation of excess Na as well as I/V D5W @ 0.5-1mEq/Lto ↓
SNa if hypernatremia dvlops over several hrs

• Advice regular cardiac pulmonary examination & SNa

monitoring for 2-4 hrs