DR HASEN ALI MIA
1st year PGT at NBMCH
Most prevalent cation in ECF(normal level of around 135- 145
Intracellular concentration of around 10mmol/L.
Responsible for 90% of total osmolality of ECF.
Major function of sodium is to maintain ECF volume and thus BP.
In normal individuals, the kidney strives to achieve Na+ balance –
that is, to have Na+ excretion equal to Na+ ingestion.
The long-term control of BP is achieved by the excretion or retention
of Na+ (and hence plasma volume) in the kidney.
Definition: Plasma Na+ concentration <135 mEq/L.
Due to a relative excess of water in relation to sodium.
Can result from excessive loss of sodium from excessive sweating,
vomiting, diarrhoea, burns, and diuretics.
It is a very common disorder, occurring in up to 22% of hospitalized
Result of an increase in circulating ADH and/or increased renal
sensitivity to ADH, combined with any intake of free water.
Patient dehydrated; reduction in total body sodium > reduction in total
NON RENAL LOSSES ( Urinary Sodium excretion < 20 mEq/L)-
Vomiting, Diarrhea, Third space losses, Pancreatitis, Burns.
RENAL LOSSES (Urinary Sodium excretion > 20 mEq/L)- The renal
causes of hypovolemic hyponatremia share an inappropriate loss of
Na+-Cl– in the urine.
Volume depletion and an increase in circulating ADH.
Causes: Reflux nephropathy, recovery phase of ATN,
diuretics,mineralocorticoid deficiency, osmotic diuresis, ketonuria.ria.
Patient has a normal store of sodium but an excess of total body water.
The most common form seen in hospitalized patients.
The most common cause Inappropriate administration of hypotonic
The syndrome of inappropriate antidiuresis is the most common
condition causing euvolemic hyponatremia.
Other causes :Glucocorticoid therapy , stress, hypothyroidism.
Most common cause of euvolemic hyponatremia.
The secretion of ADH is not inhibited by either low serum osmolality or
expanded intravascular volume.
Child with SIADH is unable to excrete water. This
results in dilution of the serum sodium and hyponatremia.
Kidney increases sodium excretion in an effort to decrease
intravascular volume to normal; thus, the patient has a mild decrease in
Diagnostic Criteria for SIADH
Renal, adrenal, or thyroid insufficiency
Heart failure, nephrotic syndrome, or cirrhosis
Urine osmolality >100 mOsm/kg (usually > plasma)
Serum osmolality <280 mOsm/kg and serum sodium <135 mEq/L
Urine sodium >30 mEq/L
Reversal of “sodium wasting” and correction of hyponatremia with
Increase in total body water > increase in total body sodium.
Patients are edematous.
RENAL CAUSES(urinary sodium > 20mEq/L): Acute or Chronic renal
NON RENAL CAUSES(urinary sodium < 20mEq/L): CHF, Cirrhosis,
Due to a measurement error which can result when the solid phase
of plasma (that due to lipid and protein) is increased.
Typically caused by hypertriglyceridaemia or paraproteinaemia.
High Osmolarity: Translocational hyponatraemia
Occurs when an osmotically active solute that cannot cross the cell
membrane is present in the plasma.
In case of insulinopaenic diabetic patient, glucose cannot enter cells
and hence water is displaced across the cell membrane, dehydrating
the cells and “diluting” the sodium in the serum.
This is also the cause of hyponatraemia seen in the TURP syndrome, in
which glycine is inadvertently infused to the same effect.
Severity of symptoms depends upon the severity of hyponatremia and
the rate at which the sodium concentration is lowered.
Acute: develops in 48 hours or less. Subjected to more severe degrees
of cerebral edema.
Chronic: develops over 48 hours and brain edema is less and is well
The signs and symptoms are due to increase in volume of ICF and
increase in volume of brain cells rather than decrease in serum sodium.
History and physical examination- to identify hypovolemic
hyponatremia (diarrhoea, vomitting, burns).
Radiologic imaging - to assess whether patient has a pulmonary or
CNS cause for hyponatremia.
Laboratory tests- Provide important initial clue in the differential
1. Plasma Osmolality
2. Urine Osmolality
3. Urine Sodium concentration
4. Uric acid level
5. Serum potassium
6. Serum glucose
Individualized considering etiology, rate of development, severity and
clinical signs and symptoms.
Hyponatremia which developed quickly needs to be treated fast
whereas slow developing hyponatremia should be corrected slowly.
GOALS of THERAPY:
1. To raise the plasma sodium concentration at a slow rate.
2. To replace sodium or potassium deficit or both.
3. To correct underlying etiology.
BASIC PRINCIPLES OF CORRECTION:
Rapid correction is indicated in acute (<48hours) symptomatic or
severe hyponatremia.(serum Na <120 mEq/L).
In chronic cases patients are at little risk, however rapid correction can
lead to demyelination. Use slower acting therapies like water
Hypovolemic hyponatremia will respond to intravenous hydration with
isotonic normal saline, with a rapid reduction in circulating AVP and a brisk
Diuretics induced hyponatremia is treated with saline and potassium
Hypervolemic hyponatremia responds to salt, water restriction (intake
< urine output), and loop diuretics .
Euvolemic hyponatremia will respond to successful treatment of the
underlying cause, with an increase in plasma Na+ concentration.
Regardless of the initial rate of correction, chosen acute treatment is
1. patient’s symptoms are abolished
2. A safe plasma sodium ( >125 mEq/L) is achieved.
1. Removal of responsible drugs- diuretics, chlorproamide etc
2. Management of physical stress or post operative pain.
3. Specific treatment of underlying cause.
4. Vasopressin antagonists (vaptans) highly effective in treating SIADH
and hypervolemic hyponatremia, reliably increasing plasma Na+
concentration as a result of their aquaretic effects (augmentation of free-
water clearance). Most of these agents specifically antagonize the V2
TO CALCULATE NEED OF REPLACEMENT SODIUM CONTAINING FLUID:
0.9% saline (154mEq/L) and 3% NaCl- hypertonic saline (513 mEq/L) are
the only two routinely used I.V. fluids . However 0.9% NS is not used to
correct hyponatremia in SIADH
GOAL : Quickly raise the sodium level but only as much as necessary to
ensure that the pt has normal respiration , seizure free and is alert.
Initial therapy – with 3% NaCl @ 4-6 ml/kg over 30-60 mints.
If no clinical improvement –another 3-4 ml/kg
Therapy stopped once child is asymptomatic or serum sodium is 125 meq/lit
Once pt is asymptomatic, remaining deficit corrected by NS.
Total body sodium defict is approximated as :
Na+ deficit(meq/lit)=(130 - serum Na+) x 0.6 x BW(kg)
Rate of rise of serum should not exceed 0.5-1 meq/lit/hr.
Rate of rise of sodium can be predicted as follows:
Rise of serum Na+/lit of fluid infused=(Inf Na+ - plasma Na+)/(0.6 x BW+ 1)
Asymptomatic or Chronic Hyponatremia
Rate of correction should be comparatively slow .
<8–10 mM in the first 24 h and <18 mM in the first 48 h
Response to isotonic saline is different in the SIADH
In hypovolemia both 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 possibly worsening the hyponatremia
Inhibits the effects of ADH
Onset of action may require up to one week
Defined as an increase in the plasma Na+ concentration to >145 mM.
Considerably less common than hyponatremia.
Associated with mortality rates as high as 40–60%.
Caused by a relative deficit of water in relation to sodium which can
1. Net water loss: Accounts for majority of cases
Pure water loss
Hypotonic fluid loss
2. Hypertonic gain: Results from iatrogenic sodium loading
Causes of Hypernatremia
Net water loss
Pure water loss
Unreplaced insensible losses (dermal and respiratory)
Neurogenic diabetes insipidus
tumors, cysts, histiocytosis, tuberculosis, sarcoidosis
aneurysms, meningitis, encephalitis, Guillain-Barre´
Congenital nephrogenic diabetes insipidus
Acquired nephrogenic diabetes insipidus
Renal disease (e.g. medullary cystic disease)
Hypercalcemia or hypokalemia
Drugs (lithium, methoxyflurane, amphotericin B, vasopressin V2-receptor
Hypotonic fluid loss
Osmotic diuresis (glucose, urea, mannitol)
Post obstructive diuresis
Polyuric phase of acute tubular necrosis
Entero cutaneous fistula
Use of osmotic cathartic agents (e.g., lactulose)
Hypertonic sodium gain
Hypertonic sodium bicarbonate infusion
Ingestion of sodium chloride
Ingestion of sea water
Hypertonic sodium chloride infusion
The symptoms of hypernatremia are predominantly neurologic.
Altered mental status is the most common manifestation, ranging from
mild confusion and lethargy to deep coma.
The sudden shrinkage of brain cells in acute hypernatremia may lead to
parenchymal or subarachnoid haemorrhages and/or subdural
Osmotic damage to muscle membranes also can lead to hypernatremic
HISTORY AND PHYSICAL EXAMINATION:
History Should focus on the presence / absence of thirst, polyuria,
and/or an extrarenal source for water loss, such as diarrhoea.
The physical examination should include a detailed neurologic
exam and an assessment of the ECFV; patients may be
hypovolemic, with reduced JVP and orthostasis.
Accurate documentation of daily fluid intake and daily urine output.
Measurement of serum and urine osmolality in addition to urine
- The appropriate response to hypernatremia and a serum
osmolality >295 mosmol/kg is an increase in circulating ADH and the
excretion of low volumes (<500 mL/d) of maximally concentrated urine,
i.e., urine with osmolality >800 mosmol/kg
A two-pronged approach:
Addressing the underlying cause.
Correcting the prevailing hypertonicity.
RATE OF CORRECTION:
Hypernatremia that developed over a period of hours (accidental
Rapid correction improves prognosis without cerebral edema.
Reducing Na+ by 1 mmol/L/hr appropriate.
Hypernatremia of prolonged or unknown duration
A slow pace of correction prudent.
Maximum rate 0.5 mmol/L/hr to prevent cerebral edema.
A targeted fall in Na+ of 10 mmol/L/24 hr,
Goal of Treatment
Reduce serum sodium concentration to 145 mmol/L.
Make allowance for ongoing obligatory or incidental losses of hypotonic
fluids that will aggravate the hypernatremia.
In patients with seizures, prompt anticonvulsant therapy and adequate
Administration of Fluids
Water ideally should be administered by mouth or by nasogastric tube
as the most direct way to provide free water, i.e., water without
Alternatively, patients can receive free water in dextrose-containing IV
solutions such as 5% dextrose.
Hypernatremia with ECF volume contraction: Isotonic
saline is given initially till ECF vol is restored. Subsequently water
deficit can be replaced with water by mouth or I.V. 5% dextrose or
Hypernatremia with increased ECF volume: Since
hypernatremia is secondary to solute administration, it can be rapidly
Patients are volume overloaded- loop diuretic is given along with
water to remove excess sodium