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