hyponatremia

2.  Total body water at birth = 75% of the wt for a term infant,which
decreases to 60% by 1 year of age up to puberty. Decreases to 50% in
females at puberty.
 TBW is divided between 2 main compartments: intracellular fluid (ICF)
and extracellular fluid (ECF). In the foetus and newborn, the ECF volume
is larger than the ICF volume.
 The ECF is further divided into the plasma water and the interstitial fluid .
The plasma water is 5% of body weight. The blood volume, given a
hematocrit of 40%, is usually 8% of body weight.
 The ICF and the ECF are in osmotic equilibrium because the cell
membrane is permeable to water.

5.  Osmolality is defined as concentration of all solutes in a given
weight of water( mosm/kg) regardless whether or not the
solutes can move across the biological membrane.
 Osmolality=2x{Na}+{glucose}/18+{BUN}/2.8
 The plasma osmolality is tightly regulated and maintained at
285-295 mosm/kg.

6.  Definition: Serum Na+ <135 meq/L
 Both total body sodium and TBW determine the serum sodium
concentration. Hyponatremia exists when the ratio of water to sodium is
increased.
 Pseudohyponatremia is a laboratory artifact that is present when the plasma
contains very high concentrations of protein (multiple myeloma, intravenous
immunoglobulin infusion) or lipid (hypertriglyceridemia,
hypercholesterolemia

8.  Mild hyponatremia : mostly asymptomatic .
 Moderate hyponatremia: Signs of raised ICT due to movement of fluids in
the ICF and leading to cell swelling
 Severe hyponatremia : Signs of raised intracranial tension like anorexia,
nausea, emesis, malaise, lethargy confusion, agitation, seizure, headache,
coma and decreased reflexes.May further lead to respiratory depression
and cheyne stokes respiration and hypothermia.
 In children with chronic hyponatremia subtle clinical features are seen.

9.  History suggestive of volume depletion :
 Diarrhea, history of diuretics use.
 Polyuria enuresis or salt craving , differentiates primary renal loss or
hypoaldosteronism.
 History suggestive of Hypothyroidism :
 Constipation, developmental delay, prolonged neonatal jaundice.
 History suggestive of adrenal insuffficiency:
 Acute illness with rapid deterioration.
 History of head injury
 History suggestive of CHF, liver diseases, renal failure,nephrotic syndrome.
 History of total intake and urine output over the last 24hours.

10.  Serum electrolytes
 Blood sugar
 Urine specific gravity
 Blood urea nitrogen.
 Serum Osmolality:
• Osmolality=2x{Na}+{glucose}/18+{BUN}/2.8
• Depending upon the calculated osmolality hyponatremia can be
 Increased osmolality - >295
• hyperglycemia, mannitol, glycerol, uremia.
 Normal osmolality - 280-295
• pseudo-hyponatremia from elevated lipids or protein
 Low osmolality - <280
• True hyponatremia.

11.  Signs of hypervolemia:
• Ascites , edema.
 Signs of hypovolemia
• Decreased pulse volume, tachycardia followed by bradycardia,decreased
skin turgor, hypotension.
 Volume status is assessed as :
 Hypovolemic hyponatremia:
 On the basis of urinary sodium excretion can be
• Non renal if urinary sodium is > 10 meq/l which is due to Emesis, diarrohea,
third space losses, burns.
• Renal if urinary sodium excretion is >20meq/|
• Loop diuretics, osmotic diuresis, obstructive uropathy,polycystic kidney
disease, proximal RTA, cerebral salt wasting, urinary tract obstruction,
hypoaldosteronism.

12.  Hypervolemic hyponatremia:
• Congestive heart failure, cirrhosis, nephrotic syndrome,renal failure,
capillary leak due to sepsis, protein loosing enteropathy
 Euvolemic hyponatremia:
• Glucocorticoid deficiency, hypothyroidism, SIADH

13. SIADH is characterized by hyponatremia, an inappropriately concentrated
urine (> 100 mOsm/kg), normal or slightly elevated plasma volume, normal-
to-high urine sodium, and low serum uric acid
 Encephalitis,
 brain tumors, head trauma,
 Pneumonia, tuberculous meningitis and sepsis.
 Postictal phase following generalized seizures.
 Seen after hypothalamic-pituitary surgery

16.  Sodium deficit:
• Sodium Deficit = TBW X (Desired serum Na' — actual serumNa)
 In asymptomatic patients, Na+ by no more than 0.5-1.0 mEq/L per h and
by less than 10-12 mEq/L over the first 24 h and less than 18 mEq/L in 48
hours.
 Acute or severe hyponatremia (plasma Na+ concentration <110-115
mEq/L) tends to present with altered mental status and/or seizures and
requires more rapid correction. Plasma Na+ concentration should be
raised by 1-2 mEq/L per hour for the first 3—4 h or until the seizures
subside. The plasma Na+concentration should be raised by no more than
12 mEq/L during the first 24 h.

17.  Though rarely seen in children.
 Children with chronic hyponatremia are most susceptible to the development of
CPM, since their brain cell volume has returned to near normal as a result of the
osmotic adaptive mechanisms described above. Therefore, administration of
hypertonic saline to these individuals can cause sudden osmotic shrinkage of
brain cells caused by correcting hyponatremia too rapidly .
 Risk factors for CPM include prior cerebral anoxic injury,hypokalemia, and
malnutrition.
 Neurologic disorder characterized by flaccid paralysis, dysarthria,and dysphagia.
 Rapid correction of sodium should be avoided.
 Sodium correction should be less than 12mEq/I per 24 hours.

18.  Hypernatremia is a [Na+ ] >145 mEq/L, although it is
sometimes defined as >150 mEq/L

19.  Iatrogenic caused by inadequate water administration or, less often, by
excessive Na+ administration
 Effects of hypernatremia on the brain by rapid correction
 Sodium intoxication by sodium bicarbonate, hyperaldosteronism
 Causes of hypernatremia from a water deficit are nephrogenic and central
diabetes insipidus
 Adipsia, the absence of thirst, is usually secondary to damage to the
hypothalamus
 Essential hypernatremia is rare in children and is thought to occur with
injury to the hypothalamic posterior pituitary axis

21.  Patients are irritable, restless, weak, and lethargic.
 Some infants have a high-pitched cry and hyperpnea
 Hypernatremia is associated with fever, hyperglycemia and
mild hypocalcemia
 As the extracellular osmolality increases, water moves out of
brain cells, leading to a decrease in brain volume = tearing
intracerebral veins (hemorrhage)

22.  Salt poisoning is associated with an elevated fractional excretion of
Na+ , whereas hypernatremic dehydration causes a low fractional
excretion of Na+
 As hypernatremia develops, the brain generates idiogenic osmoles to
increase the intracellular osmolality and prevent the loss of brain water
THUS IF the serum [Na+ ] is lowered rapidly, there is movement of water
from the serum into the brain cells leading to brain swelling manifested
as seizures or coma
 Child with central diabetes insipidus should receive desmopressin acetate
because this treatment reduces renal excretion of water
 Desmopressin acetate in children are for the management of central
diabetes insipidus and nocturnal enuresis

23.  As hypernatremia develops, brain generates idiogenic osmoles to
increase intracellular osmolality and prevent loss of brain water.
 Chronic hypernatremia should not be corrected rapidly.
 Loop diuretic increases the removal of excess Na+ and water so
decreasing risk of volume overload.
 With Na+ overload, hypernatremia is corrected with Na+ free
intravenous fluid(D5W).
 Child with central diabetes insipidus should receive desmopressin
acetate.

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