approach to hyponatremia in children
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Transcript of approach to hyponatremia in children
Approach to Hyponatremia
Moderator: Dr. Swati Pakolu
Ranvijay Rana
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.
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.
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
Hyponatremia PseudohyponatemiaHyperglycemiaMannitolHypovolemic hyponatremia
Euvolemic•SAIDH
•Glucocorticoid deficiency•Hypothyroidis
m•Water
intoxication•Nephrogenic
SAIDH
Hypervolemic•Congestive cardiac
failure•Cirrhosis
•Nephrotic syndrome•Capillary leak•Protein loosing
enteropathy
Hypovolemic
Causes of hyponatremia
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
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.
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.
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.
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.
Hypervolemic hyponatremia: Congestive heart failure, cirrhosis, nephrotic syndrome,
renal failure, capillary leak due to sepsis, protein loosing enteropathy
Euvolemic hyponatremia: Glucocorticoid deficiency, hypothyroidism, SIADH
SIADHSIADH 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
Diagnostic criteria for SIADH
Clinical parameters
SAIDH Cerebral salt wasting
Central DI
Serum sodium Istatus
LOW Low High
Urine output NORMAL high High
Urine sodium HIGH Very high Low
Intravascular volume
NORMAL Low Low
Vasopressin level
HIGH low low
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.
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.
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.
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 ?
Thank you