Fluid and Electrolyte Therapy in paediatrics Hypo and hypercalcemia Hypo and hypernatremia Hypo and hypermagnesemia

1. Fluid and Electrolyte Therapy in
Infants and Children
Dr Raseena vattamkandathil
MEM Resident

2. Why Dehydration..?
High percentage of total body
water
Decreased ability to control
water loss
Decreased ability to concentrate
the urine

3. TYPES OF DEHYDRATION
1. Isonatremic (isotonic) dehydration - MC
2. Hyponatremic (hypotonic) dehydration
3. Hypernatremic (hypertonic) dehydration

4. HISTORY
● Symptoms? what they are? when they started? where they started?
e.g., was the child in a hot environment?
● Whether fever is present?
● Tachypneic? and prior treatment.?

5. Breast feeding history
 Frequency of feeds
 Whether the mother feels she has good milk production
 Whether the infant is feeding or engaged in
nonnutrient sucking for comfort.
 If not breastfeeding, ask what type of fluid has been
Given- hypotonic fluids (e.g., water) increase the risk of
hyponatremia.

6. BOTTLE FED INFANTS
● Whether the formula is premixed or made from
powder
● hypernatremia or hyponatremia can result from inappropriately prepared
formula.

7. ASSESS OUTPUT
● Questions surrounding output aid in assessing whether replacement of losses has been
adequate
● Excess output results from vomiting or diarrhea (quantify the frequency and volume if
possible).
● Assess urine output by asking how often the child is urinating
● The number of wet diapers if the child is not yet toilet trained.

8. Inquire about volume status
● Ask about tear production
● The presence or absence of sweat
● Child’s general appearance
● Mental status: is the child increasingly irritable or lethargic?
● Has the parent noticed a change in the skin (cyanotic, pale, mottled)?

9. ● Ask about signs or symptoms of infection
● Recent travel, sick contacts
● Underlying chronic disease, which may point to a specific cause of
dehydration.
● Children are at risk for accidental ingestion of toxins or plants, many of
which can cause vomiting and lead to electrolyte disturbances.

10. Most important, is a change in weight, because weight loss
is the gold standard for assessment of volume status

11. On examination..
● Tachycardia is an early sign of dehydration
● Tachypnea - metabolic acidosis
● Mental Status and the presence of lethargy or hypotonia - severe dehydration or
electrolyte abnormalities.
● Infants- fontanelle
● Presence or absence of tears when crying
● Mucous Membranes - cracked, dry lips or decreased saliva in the mouth

12. ● Temperature, colour, and turgor of the skin
● Capillary refill time- less than 2 seconds when normal.
● Character of the pulses - diminished pulses in significant dehydration.

13. ‘’Perform a bedside glucose test in any child presenting with altered
level of consciousness, and rapidly correct hypoglycaemia’’

14. NASOGASTRIC VS IV HYDRATION
● For children unable to tolerate oral rehydration, nasogastric hydration is effective,
even in vomiting patients.
● Nasogastric treatment is more cost effective than IV treatment.

15. “In a large study comparing nasogastric hydration versus IV hydration over 3 hours,
subjects in the nasogastric-treated group had fewer complications, achieved resolution of
ketonuria more often, and had greater reduction in specific gravity than IV-treated
subjects”

16. INITIAL TREATMENT OF DEHYDRATION

17. MODERATE AND SEVERE DEHYDRATION
● The child unable to tolerate oral/nasogastric rehydration therapy or with severe
dehydration requires prompt fluid resuscitation with large volumes of fluid over a short
period of time
● Give 20 mL/kg boluses over 5 to 10 minutes repetitively until hemodynamic
stabilization
● Up to 60 mL/kg or more may be required in the 1st hour, unless contraindicated

18. ● Use an isotonic solution such as 0.9% saline or a lactated Ringer’s
solution during this resuscitation phase.
● After initial volume expansion, continue replacement with either normal
saline or 5% dextrose

20. The Formula for daily fluid requirements
● For the first 10 kg: 100 mL/kg/d (4 mL/kg/h)
● For the second 10 kg: 50 mL/kg/d (2 mL/kg/h)
● For each kg >20 kg: 20 mL/kg/d (1 mL/kg/h)

21. “Because hyponatremia is the most common intragenic complication of IV
fluid therapy, it is important that isotonic solutions be used as maintenance
fluid, such as normal saline with 5% dextrose”

22. Discharge criteria
1. Appears clinically well, alert, and orientated
2. Vital signs within normal limits for age
3. Urine output during hydrating period
4. Intake is equal or greater to ongoing losses

23. HYPONATREMIA

25.  First determine if a low sodium value is a true value by relating the
sodium value to the osmolarity.
 If hyponatremia occurs in a hyperosmolar state - osmotically active solute
in the plasma such as excess glucose or alcohol.
 If hyponatremia occurs in the presence of normal osmolarity-
hyperlipidemia or hyperproteinemia- correct the underlying disorder rather
than the serum sodium level.
 When hyponatremia occurs in a hypo-osmolar state - excess of free water
or loss of sodium.

26. CLINICAL FEATURES
 Signs and symptoms of hyponatremia depend on the serum sodium level and
the speed at which the sodium level falls.
 Symptoms primarily involve the CNS
 Neurologic symptoms: nausea, vomiting, headache, mental status changes,
altered consciousness, diminished reflexes, hypothermia, pseudobulbar
palsy, and seizures.
 Musculoskeletal symptoms: weakness, muscle cramps, and lethargy.

27.  Although patients may be only mildly symptomatic with sodium levels as low
as 120 mEq/L if the low level is chronic (>48 hours), symptoms usually occur
with an acute drop in serum sodium level below 120 mEq/L.
 Without appropriate treatment, complications include respiratory failure,
seizures, and death.

29.  Treatment depends on the stability of the patient and associated symptoms.
 Rapid correction can cause severe demyelination of brainstem neurons.
 If severe neurologic symptoms, such as confusion, altered level of consciousness, or
seizures, typically with sodium level <120 mmol/L - a rapid, controlled increase in sodium
level is required until neurologic symptoms resolve or a sodium level of 120 mmol/L is
achieved.

30. ● For euvolemic hyponatremia, after correction of serum sodium level, begin water
restriction and treat the underlying disorder.
● For hypervolemic hyponatremia (edema), start sodium and water restriction and
administer diuretics if needed to treat the clinical condition

31. HYPERNATREMIA
 Hypernatremia is a serum sodium level >145 mEq/L.
 Because of dehydration
 secondary to excessive sodium intake
 if free water is limited or if the formula is mixed improperly.

32. ● Serum sodium levels of >160 mEq/L require immediate attention due to
the potential for serious complications and permanent neurologic sequelae
● Patients who have a sodium level of <160 mEq/L and receive treatment
typically have symptoms that are relatively mild and self-limited.

33. CLINICAL FEATURES
 Signs and symptoms of hypernatremia result from cellular dehydration
 Mental status changes, muscular weakness, ataxia, tremors, hyperreflexia,
seizures, unresponsiveness, intracerebral hemorrhage, permanent neurologic
dysfunction, and death.
 Increased peripheral tone with brisk reflexes, muscle weakness, high-pitched
cry, nuchal rigidity, myoclonus, asterixis, chorea, altered level of consciousness,
or seizures

34. ● Correct serum sodium gradually to avoid cerebral edema and associated
central pontine myelinolysis
● Closely monitor serum sodium levels every hour initially to ensure that the
level is reduced no faster than 1 mEq/L/h and no more than 15 mEq/L in
the first 24 hours.

36. ● Monitor urine output given the risk of acute tubular necrosis
● Correct underlying causes.
● Hypervolemic hypernatremia may require dialysis if sodium levels cannot be
decreased without volume overload.
● Dialysis may also be required for hypernatremia of any type if the initial serum
sodium is >180 mmol/L.

37. Hypokalemia
● Most commonly occurs secondary to profuse vomiting and/or diarrhea.
● Therapy with loop or thiazide diuretics, mineralocorticoids, or laxatives and
diabetic ketoacidosis.
● In diabetic ketoacidosis, profound hypokalemia can result from osmotic diuresis,
although in the face of the hydrogen–potassium shift that accompanies acidemia,
serum levels may be normal or falsely elevated.

38. Uncommon causes of hypokalemia
 Renal tubular acidosis
 Bartter’s or Gitelman’s syndrome
 Cushing’s syndrome
 Familial hypokalemia-induced paralysis.

39. CLINICAL FEATURES
● In most cases, hypokalemia occurs slowly, and thus patients are asymptomatic.
● Clinical signs tend to reflect the rate of fall of serum potassium rather than the
absolute level.
● Severe potassium depletion can result in skeletal muscle weakness, ileus, and
cardiac conduction disturbances.
● A prominent ECG manifestation is the U wave.

41. HYPOCALCEMIA
▪ Serum calcium level <8 milligrams/dL (2 mmol/L) or
▪ Ionized calcium level <4.4 milligrams/dL (1.1 mmol/L);

42. CAUSES
Hypoparathyroidism
 Idiopathic
 DiGeorge’s syndrome
 after thyroid surgery
 associated with magnesium
deficiency.
End-organ resistance to
parathyroid hormone.
 Associated with vitamin D
deficiency.

43.  Dietary deficiency
 Chronic renal failure.
 Young infants fed cow’s milk, which is high in phosphate, can develop
severe hypocalcemia.
 hyperventilation: the decreased Pco2 results in an acute respiratory
alkalosis that rapidly decreases levels of ionized calcium.

44. Clinical features
 Muscle weakness, vomiting, and irritability.
 Infants may simply appear “jittery.”
 In severe cases, tetany, laryngospasm, carpopedal spasm, and seizures can
occur.
 Carpopedal spasm is especially common in children with hyperventilation
syndrome.

46. “The most characteristic ECG abnormality of hypocalcemia
is a prolonged QT interval”

47. INVESTIGATION
 Total serum and ionized calcium, phosphate
 Total protein and albumin
 Parathyroid hormone
 BUN, and creatinine levels.
 Urine calcium level should also be collected.
 In neonates, a chest radiograph should be done to look for a thymic shadow in infants and
young children. If the thymus is not present, consider DiGeorge’s syndrome.

48. TREATMENT
 Calcium gluconate 10% in a dose of 100 milligrams/kg at a rate not to
exceed 100 milligrams/min, with continuous ECG monitoring

49. HYPERCALCEMIA Etiology
 Malignancy involving the lymphoreticular system.
 Vitamin A or D intoxication
 Hyperparathyroid syndromes
 Hyperthyroidism
 Adrenal Insufficiency
 Pheochromocytoma

50. Clinical features
 Hypotonia
 Fatigue, irritability, anorexia
 Vomiting, and constipation.
 Affected children may be clinically dehydrated and complain of polyuria
and/or polydipsia.
 An ECG may reveal bradycardia and a shortened QT interval.

51. INVESTIGATIONS
 Total Serum and ionized calcium levels
 CBC
 Total protein and albumin
 Alkaline phosphatase levels.
 An evaluation of the vitamin D level may also be indicated, depending on
the patient’s medical history

52.  Acutely, patients with functioning kidneys can be treated with aggressive
IV hydration with or without furosemide, 1 to 2 milligrams/kg IV, to a
maximum of 40 milligrams.
 Then, treat the underlying cause

53. HYPOMAGNESEMIA ETIOLOGY
 GI loss : Diarrhea, malabsorption
short gut, and fistulas
 Hyperaldosteronism
 Iatrogenic causes of renal loss :
• Osmotic diuretics
• parenteral fluids
• Antibiotics
• Chemotherapeutics
 DM
 Disorders of the
parathyroid glands

54. “Hypercalcemia may cause magnesium loss as well as
hypophosphatemia”

55. CLINICAL FEATURES
 Hypocalcaemia like symptoms : muscle spasms, weakness, or even
atrophy
 CNS symptoms include ataxia, abnormal movements, nystagmus, and
seizures
 Cardiac changes - prolonged PR and QT intervals and may predispose to
arrhythmias such as torsades de pointes.

56. TREATMENT
 In symptomatic patients give IV magnesium sulfate, 25 to 50 milligrams/kg as
10% solution over 30 minutes, and repeat every 4 to 6 hours as needed.
 Include magnesium in parenteral or enteral nutritional liquids in chronically ill
children

57. HYPERMAGNESEMIA
 Hypermagnesemia is rare.
 Serum levels of >2.2 mEq/L are considered elevated.
 The most common cause is ingestion of exogenous magnesium, typically
found in antacids and laxatives.
 Patients with renal dysfunction are at increased risk.

58. CLINICAL FEATURES
 Hypotension
 loss of deep tendon reflexes
 respiratory failure.
 Cardiac manifestations include widening of the QRS, PR, and QT intervals.

59.  Treatment is removal of exogenous sources
 hydration accompanied by diuresis.
 Severe symptoms may be mitigated with IV calcium, 0.5 mL/kg delivered
as calcium gluconate.
 Dialysis is effective in patients with renal failure.

61. ………….THANK YOU