hyponatremia in children

1. Approach to
Hyponatremia
Moderator: Dr. Swati Pakolu
Ranvijay Rana

2. Basic concepts:
 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
 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. Hyponatremia Defined
 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

7. Hyponatremia Pseudohyponatemi
a
Hyperglycemia
Mannitol
Hypovolemic
hyponatremia
Euvolemic
•SAIDH
•Glucocorticoi
d deficiency
•Hypothyroidis
m
•Water
intoxication
•Nephrogenic
SAIDH
Hypervolemic
•Congestive cardiac
failure
•Cirrhosis
•Nephrotic syndrome
•Capillary leak
•Protein loosing
enteropathy
Hypovolemic
Causes of hyponatremia

8. Extra renal losses
•Emesis
•Diarrohea
•Third space losses
•burns
Renal losses
•Loop diuretics
•Osmotic diuresis
•Obstructive uropathy
•Polycystic kidney disease
•Proximal RTA
•Cerebral salt wasting
•Urinary tract obstruction
•Hypoaldosteronism

9. Clinical features:-
 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.

10. Primary history taking:
 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 24
hours.

11. Basic analysis:
 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.

12. Volume status:
 Signs of hypervolemia:
 Ascites , edema.
 Signs of hypovolemia
 Decreased pulse volime, tachcardia 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/l
 Loop diuretics, osmotic diuresis, obstructive uropathy,
polycystic kidney disease, proximal RTA, cerebral salt
wasting, urinary tract obstruction, hypoaldosteronism.

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

14. SIADH
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

15. Diagnostic criteria for SIADH

16. Clinical
parameters
SAIDH Cerebral salt
wasting
Central DI
Serum sodium I
status
LOW Low High
Urine output NORMAL high High
Urine sodium HIGH Very high Low
Intravascular
volume
NORMAL Low Low
Vasopressin
level
HIGH low low

17. Treatment:
 Sodium deficit:
 Sodium Deficit = TBW X (Desired serum Na+
– actual serum
Na+
)
 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.

18. Central pontine myelinosis
 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/l per 24 hours.

19.  A 2 year old male child presented with history of seizure with
no history of fever, loose stools and a serum electrolyte report
showing serum sodium of 122 mEq/l.
 How to approach the child.

20. Clinical scenario
 A 2 year old male child presented with history of
fever and loose stools since 4 days.Child had history of
decreased urine output.
 On examination had severe dehydration with
thready pulse.
 On investigation serum sodium was 122 mEq/l.
 How do you approach the child ?

21.  Thank you