SODIUM DISORDERS

Sodium is the principle cation in extracellular fluid, responsible for maintenance of osmolality in intravascular and interstitial fluid compartments. About 45% of total body sodium is present in body fluids, rest being in bones, cartilages and connective tissues.

Physiology: Kidney is the prime regulator of sodium balance in body. While sodium is freely filtered through glomeruli, ~2/3^rd of it is reabsorbed in proximal tubules and loop of Henle. Remaining sodium is also reabsorbed in distal tubules and collecting ducts and only lt;1% of filtered sodium is actually excreted in urine. Renal reabsorption of sodium is an active process, facilitated by renin-angiotensin mechanism and aldosterone secretion; and opposed by the atrial natriuretic hormone.

Hyponatremia is the commonest electrolyte abnormality in hospitalized children, defined as S. sodium levels lt;135 mEq/L, though it is rarely symptomatic till levels fall lt;125 mEq/L.

Causes: Gastrointestinal loss in diarrhea or vomiting is the commonest caus of hyponatremia in children, apart from other causes (Table 7.5). In critically sick

TABLE 7.5: Causes of hyponatremia

TABLE 7.6: Causes of hypernatremia

Primary sodium deficit:

Extra-renal losses

GIT: Diarrhea, vomiting, nasogastric drainage

Skin: Burns, cystic fibrosis

Third space: Paralytic ileus

Renal losses

Prematurity: Poor concentration capability

Forced diuresis: Diuretics, diabetes mellitus

Renal: Renal tubular acidosis, acute tubular necrosis

Adrenal: Congenital adrenal hyperplasia (salt-loosing)

Disproportionate water retention:

Syndrome of inappropriate ADH secretion (SIADH)

Excess intake: Psychogenic, Na⁺ free IV fluids

Renal: Nephrotic syndrome, renal failure

Congestive cardiac failure

Pseudo-hyponatremia due to hyperlipidemia

Nephrotic syndrome

Diabetic ketoacidosis

children, excess ADH secretion, i.e.

Etiologically, hyponatremia is also classified as:

• Hypovolemic hyponatremia with sodium loss in excess of the fluid loss due to renal or extrarenal losses;

• Normovolemic or euvolemic hyponatremia with pro­portionate loss of sodium and water, e.g. in SIADH or due to drugs, e.g. cyclophosphamide, vincristine, carbamazepine, etc;

• Hypervolemic hyponatremia due to excess water retention, e.g. in CCF, nephritic syndrome, cirrhosis, renal failure, etc.

Pathophysiology: Hyponatremia leads to decreased ECF osmolarity and consequent movement of water from ECF to ICF, leading to cellular edema including cerebral edema. Brain also attempts to adapt hyponatremia by extrusion of intracellular electrolytes and osmolytes (glutamine, aspartate, etc.), which are neuroexcitatory and can produce seizures, even without cerebral edema. Clinically, symptomatic hyponatremia predominantly presents with signs of cerebral edema, e.g. altered sensorium and seizures. Severe cases may also present with hypertension, pulmonary edema and heart failure.

Hyponatremic encephalopathy is relatively more common in children than adults due to larger brain size (versus intracranial volume) and may lead to irreversible brain damage, if left untreated.

Asymptomatic prolonged hyponatremia in preterms may lead to poor growth, development and sensorineural hearing loss.

Treatment of hyponatremia depends on the cause, severity and duration:

• Asymptomatic or dilutional hypernatremia, e.g. in SIADH, does not require specific correction except fluid restriction and treatment of primary cause.

Increased sodium intake:

• Concentrated ORS or formula feeds

• Hypertonic IV fluids

• Near-drowning in sea water

• Use of common salt for emesis

• Intentional salt poisoning

Relative water deficit:

• Diabetes insipidus

• Diabetes mellitus

• Gastroenteritis

• Reduced oral intake—intentional, psychogenic

• Increased insensible loss—respiratory distress

• Acute symptomatic hyponatremia should be treated with IV 3% NaCl as a bolus of 2 ml/kg over 10-15 minutes (or 3-5 ml/kg over first hour), which may be repeated to maximum 100 ml, till the symptoms resolve. Serum sodium level should be monitored every 2 hours, with an objective to raise them by ~5-6 mEq/L in first 1-2 hours.

• Chronic or left-over hyponatremia after acute correction should be treated more slowly with IV 3% NaCl, in doses calculated with following formula:

Sodium deficit (mEq) = (125 - actual S. sodium) ? body weight ? 0.6 Whereas 125 is desired Na⁺ level and 0.6 is distribution coefficient of sodium in body.

Rapid correction of hyponatremia should be avoided to prevent pontine/ extra-pontine osmotic myelinolysis, once serum sodium levels approach 125 mEq/L and no more than 10 mEq/L deficit should be corrected in 24 hours. As a thumb rule, 12 ml/kg of 3% NaCl raises S. Na⁺ levels by ~10 mEq/L.

Hypernatremia is relatively less common than hypo­natremia, defined as serum sodium levels gt;145 mEq/L. Causes: Hypernatremia in children is usually iatrogenic in origin, due to use of concentrated oral rehydration/ parenteral fluids. Concentration hypernatremia is seen in disorders with excessive water loss, e.g. diabetes insipidus (Table 7.6).

Pathophysiology: Hypernatremia increases osmolarity of the ECF, leading to movement of water from ICF to ECF and consequent cellular dehydration. In acute severe hypernatremia, this osmotic shift may lead to shrinkage of the brain, tearing of meningeal vessels and intracranial hemorrhage.

Clinically hypernatremia present with features of cellular dehydration. Increased thirst is the earliest compensatory response and clinical indicator to deve­loping hypernatremia, followed by:

• Neurological signs, e.g. irritability, twitching and seizures.

• Skin signs, e.g. dry skin with typical doughy consis­tency, which may mask signs of dehydration.

Thrombotic complications due to intracellular dehydration and consequent hypercoagulability may develop in severe cases, including strokes, renal vein thrombosis and deep vein thrombosis.

Investigations: All cases of hypernatremia should be assessed for serum and urine osmolality and urinary sodium, along with blood urea, serum creatinine and electrolytes.

Treatment: Hypernatremia is generally well tolerated as brain generates idiogenic osmols to increase the intracellular osmolarity. Rapid correction of hyper­natremia should be avoided to prevent sudden decrease in ECF osmolarity, which may lead to rapid movement of water within the cells and consequently cause cerebral edema with seizures, pulmonary edema and congestive cardiac failure. As general rule, the rate of sodium correction should never exceed 0.3-0.5 mEq/L per hour or 8-12 mEq/L per day.

Important considerations in correction of hyper­natremia include:

• Recommended IV fluid is N/2 saline in DW 5% (with added 20 mEq/KCl after passage of urine). Sodium-free fluids should never be used to avoid rapid correction.

• Replacement fluid volume should be ~1.5 times of maintenance requirement + deficit correction as 3-4 ml/kg for each mEq/L of serum Na⁺ above 145 mEq/L, infused over recommended period. Ongoing losses should be added as required. Oral rehydration should be started as early as possible.

• Sodium levels should be monitored every 1-2 hourly to limit the rate of fall lt;0.5 mEq/L/hour.

• If child develops seizures due to rapid correction, administer 3% Nacl 4-6 ml/kg over 30 minutes.

• Peritoneal dialysis is indicated for serum Na⁺ exceeds 180 mEq/L, using high glucose-low sodium dialysate.

• In cases presenting with hypotension/shock on admission, hypernatremic correction should start after one or two boluses of 20 ml/kg. Normal saline over 20 minutes for restoration of intravascular volume.

7.3