Common electrolyte Imbalance in pediatrics

common electrolyte disturbance

1. Electrolyte Imbalance Sodium hyponatremia hypernatremia Potassium hypokalemia hyperkalemia

2. sodium Sodium is the dominant cation of the ECF and it is the principal determinant of extracellular osmolality. More than 40% of total body sodium is in bone. The low intracellular Na concentration(10 mEq /L) is maintained by Na+,K +-ATPase . Its concentration determined by water balance instead of sodium balance. When Na con c ↑ → ↑osmolality → ↑ secretion of ADH↓ → renal water conservation → Na con c returns to normal and vice versa

3. intake readily absorbed throughout the gastrointestinal tract. breast milk (≈7  mEq /L) Mineralocorticoids↑ Na transport glucose enhances sodium absorption Excretion Stool, sweat(minimal) Urine(main) determined by effective plasma volume

4. Hypernatremia sodium concentration >145 mEq /L, although it is sometimes defined as >150 mEq /L Moderate or severe hypernatremia has significant morbidity, including the risks of overly rapid correction. Brain hemorrhage is the most devastating consequence of hypernatremia leading to seizures and coma

5. pathophysiology 3 basic mechanisms Excessive sodium usually iatrogenic in a hospital setting as a result of correction of metabolic acidosis with sodium bicarbonate. Hyperaldosteronism Water deficit nephrogenic and central diabetes insipidus Prematurity (↑water loss) Ineffective breast-feeding Adipsia (the absence of thirst) Water and sodium deficits Diarrhea (inadequate intake because of emesis, lack of access to water, or anorexia.) Diuretics, DM, CKD

6. Clinical Manifestation Dehydrated( sunken eyes , ↑ thirst, irritable, prolonged skin fold) Failure to thrive (breast fed infants) CNS symptoms (irritable, restless, weak, and lethargic, high-pitched cry and hyperpnea ) hyperglycemia and mild hypocalcemia CSF protein is often ↑ in infants with significant hypernatremia due to leakage from damaged blood vessels. Thrombotic complications in severe hypernatremic dehydration(stroke, dural sinus thrombosis, peripheral thrombosis, and renal vein thrombosis)

7. Diagnosis Urine analysis Osmolality electrolytes Serum Na RFT

8. Management Water deficit Treat underlying cause Monitoring

9. hypernatremia should not be corrected rapidly. Goal of treatment- to decrease the serum sodium by <12 mEq /L every 24 hr , a rate of 0.5 mEq /L/hr. As hypernatremia develops, the brain generates idiogenic osmoles to increase the intracellular osmolality and prevent the loss of brain water. most prominent when hypernatremia has developed gradually. If the serum Na concentration is lowered rapidly, there is movement of water from the serum into the brain cells to equalize the osmolality. The resultant brain swelling manifests as seizures or coma

10. In a child with hypernatremic dehydration the first priority is restoration of intravascular volume with isotonic fluid . Normal saline(10-20 mL/kg) is preferable to lactated Ringer solution because the lower sodium concentration of ringer can cause the serum sodium to decrease too rapidly, especially if multiple fluid boluses are given.

11. Water deficit The sodium concentration of the deficit replacement fluid, the rate of fluid administration, and the presence of continued water losses determine the rate of decrease of the sodium concentration. The following formula is often cited for calculating the water deficit: water deficit= body weight × 0.6(1-[145/current Na])

12. Alternative approach —based upon the observation that the administration of 3 mL of electrolyte-free water per kilogram of lean body weight given will lower the serum sodium by approximately 1 meq /L . which is nearly identical to the deficit calculated from the water deficit formula.

13. With sodium overload, hypernatremia is corrected with sodium-free intravenous fluid (5% dextrose in water [D5W]). When hypernatremia is due to sodium intoxication peritoneal dialysis allows for removal of the excess sodium. Hyperglycemia from hypernatremia is not treated with insulin because the acute decrease in glucose may precipitate cerebral edema by lowering plasma osmolality

14. Treat underlying cause diabetes insipidus - desmopressin acetate Diarrhea Decrease salt intake

15. Hyponatremia Hyponatremia is a serum sodium level <135 mEq /L ratio of water to sodium is increased. can occur with low, normal, or high levels of body sodium. Similarly, body water can be low, normal, or high.

16. Etiology Hyperosmolarity (hyperglycemia) Extrarenal loss(GI, skin) Renal loss(diuretics, ATN, salt wasting) Euvolumic hyponatremia (SIADH, water intoxication) Hypervolumic hyponatremia

17. pathogenesis In hypovolumic hyponatremia the volume depletion (Diarrhea and emesis due to AGE, burns) Stimulates ADH synthesis, resulting in renal water retention. decreases the GFR and enhances water resorption Hypoaldosteronism In hypervolemic hyponatremia increase in water is greater than the increase in sodium

18. Clinical Manifestations Apnea Neurologic symptoms- anorexia, nausea, emesis, malaise, lethargy, confusion, agitation, headache, seizures, coma, and decreased reflexes (due to brain swelling) muscle cramps and weakness( rhabdomyolysis in water intoxication.)

19. Diagnosis history points to a likely etiology Plasma osmolality Serum Na RBS RFT Urine analysis

20. Management based on the pathophysiology of the specific etiology avoid “overly rapid” correction. avoid correcting con c by >12 mEq /L/24 hr or > 18 mEq /L/48 hr. correction of hyponatremia may cause central pontine myelinolysis (CPM). This syndrome, which occurs within several days of rapid correction of hyponatremia , produces neurologic symptoms, including confusion, agitation, flaccid or spastic quadriparesis , and death.

21. In hypovolemic hyponatremia - restore the intravascular volume with isotonic saline →suppresses ADH production → excretion of the excess water Sodium deficit = Total body water x (desired SNa – actual SNa )

22. In hypervolemic hyponatremia water and sodium restriction Vasopressin antagonists ( tolvaptan ), In severe salt and water overload associated with renal failure, dialysis In isovolumic hyponatremia hypertonic saline Restrict water intake Give aprropriate formula

23. iatrogenic hyponatremia due to the administration of hypotonic intravenous fluids should receive 3% saline if they are symptomatic

24. Potassium Most abundant in the ICF (150  mEq /L) Normal serum level 0.4  mEq /L The majority of body potassium is contained in muscle.(↑as the muscle mass increases) chemical gradient resulting from Na + ,K + -ATPase produce resting membrane potential of cells

25. Intake plentiful in food 90% of ingested K absorbed in the intestine(mostly SI) Excretion Some sweat Through colon Urine (major) facilitated by aldosterone Increased in alkalosis Decreased by insulin

26. Hyperkalemia Very alarming electrolyte abnormality due to its potenial for lethal arrhythmia due to Adrenal disorders causing hypoaldosteronism Inadequate renal excretion Medication Increased intake Transcellular shift(acidosis, DM, rhabdomyolysis )

27. Fictitious or spurious hyperkalemia- due to hemolysis during a heelstick or phlebotomy, but it can be the result of prolonged tourniquet application or fist clenching→ local potassium release from muscle.

28. Clinical Manifestations Due to role of potassium in membrane polarization Chest pain, palpitations, dyspnea v/s- bradycardia , tachypnea Cardiac signs precede peaking of the T waves, ST-segment depression, increased PR interval, flattening of the P wave, and widening of the QRS complex, ventricular fibrillation, asystole fasciculations , muscle weakness, and even an ascending paralysis

29. Diagnosis History medications, diet and dietary supplements, risk factors for kidney failure, reduction in urine output, blood pressure, and volume status physical examination signs of arrhythmia electrolytes, RFT serum osmolality a complete blood count urinary pH. A urine Na+ concentration <20 mM indicates that distal Na+ delivery is a limiting factor in K+ excretion

30. Management stop all sources of additional potassium (oral, intravenous) The plasma potassium level, the ECG, and the risk of the problem worsening determine the aggressiveness of the therapeutic approach the potassium level is >6.0-6.5  mEq /L, an ECG should be obtained to help assess the urgency of the situation

31. 2 basic goals: to stabilize the heart- Calcium to remove potassium from the body Na- sodium bicarbonate if metabolic acidosis Insulin to shift K in to cell with glucose to prevent hypoglycemia Nebulized albuterol Promote K loss: Kayexalate , diuretics, dialysis

32. Hypokalemia Serum k level <3.5mmol/L common in children, with most cases related to gastroenteritis. Etiology Spurious High WBC Decreased intake Anorexia nervosa Intracellular shift Alkalosis, insulin, drugs, refeeding syndrome Increased loss(renal extra renal) Diarrhea, sweating, Kayexalate ingestion( extrarenal ) In acid base dsturbances ,

33. Clinical Manifestation Constipation, distention Exercise intolerance Dyspnea Urinary retention polyuria and polydipsia Rarely muscle paralysis (at <2.5  mEq /L) Poor linear growth ECG changes ( flat T wave, rising U wave, arrhythmias) Hyperglycemia ( impaired insulin release)

34. diagnosis history- diet, gastrointestinal losses, and medications Serum electrolyte Urine electrolyte ECG

35. management Potassium supplementation(cautious if renal function decreased potassium deficit varies with severity of hypokalemia Oral K safer but not as rapid ( 2-4  mEq /kg/day , max of 120-240  mEq /day in divided doses IV cautious of hyperkalemia( 0.5-1  mEq /kg, given over 1  hr ) Spironolactone ( aldosterone antagonist) Potassium sparing diuretics ( amiloride , triamterene)for patients with excessive urinary losss ) If hypokalemia, metabolic alkalosis, and volume depletion are present restoration of intravascular volume with adequate NaCl will decrease urinary K+ losses