This document discusses sodium homeostasis and hyponatremia and hypernatremia in children. It defines hyponatremia and hypernatremia and describes their most common causes in children, which include excess free water retention leading to hyponatremia and failure to replace water losses leading to hypernatremia. The document outlines approaches to evaluating and managing hyponatremia and hypernatremia based on the child's volume status and underlying condition. Management involves fluid restriction, sodium supplementation, and treating the underlying cause while avoiding too rapid of sodium correction.

1. SODIUM
HOMEOSTASIS
Dr abdullah alzahrani

2. Hyponatremia
• serum or plasma sodium less than 135 mEq/L.
• most common electrolyte abnormalities in children.
• true incidence of pediatric hyponatremia is unknown, as
published data are based on hospitalized children.
• In a study from the United States of 1048 children who
had normal serum sodium levels at the time of
presentation, 35 percent of the cohort developed
hyponatremia .
• Patients who received hypotonic fluids were more likely
to develop hyponatremia than those who received isotonic
fluids (39 versus 28 percent)

3. Hyponatremia: Etiology
• Plasma tonicity is regulated by the release of
(ADH) promoting water retention, and by thirst-
prompting water ingestion.
• In children, the underlying pathogenesis for
hyponatremia is typically due to excess free water
retention
• Hypovolemia
• Normovolemia
• Hypervolemia

4. Hyponatremia: hypovolemia
• Gastrointestinal losses : most common , appropriate
elevation in ADH, when hypotonic fluids are
administered, free water is retained in excess of solutes
resulting in more hyponatremia.
• Skin loss of sodium and water results in volume
depletion, leading to free water retention and
hyponatremia. especially in patients with cystic fibrosis.
• Third space
• Intense exercise : High rate of fluid consumption

5. Hyponatremia: hypovolemia
Renal salt wasting:
• Cerebral salt wasting: intracranial surgery, meningoencephalitis,
and head injury.
• Primary renal tubular disorders: Bartter and Gitelman
syndromes.
• Disorders of adrenal insufficiency: 21-hydroxylase deficiency
and hypoaldosteronism
• Diuretic: thiazide diuretic, which acts in the renal cortex at the level
of the distal tubule, thereby not interfering with medullarly ADH-
induced water retention.

6. Hyponatremia: normovolemia
• Syndrome of inappropriate ADH secretion
• in normal condition, excess water intake lowers tonicity that
suppresses ADH release, allowing for free water excretion.
• persistent ADH release and water retention in normovolemic
children can be seen in a number of disorders.
• Primary polydipsia

7. Causes of ADH release
• Physiologic
• Hypovolemia, hyperosmolality
• Pulmonary
• Pneumonia, bronchiolitis, asthma, pneumothorax, cystic fibrosis,
positive pressure mechanical ventilation
• Central nervous system
• Meningitis, encephalitis, CNS tumor, brain trauma, pain, anxiety,
hypoxia
• Endocrine
• hypothyroidism and cortisol deficiency
• Medication effect
• cyclophosphamide, vincristine, valproate and carbamazepine

8. Hyponatremia: hypervolemia
• Effective arterial blood volume depletion
• total body volume overload manifested by edema, but decreased
effective circulating volume (ECV), leads to ADH release resulting
in free water retention, and stimulation of the renin-angiotensin-
aldosterone axis resulting in low urinary sodium excretion.
• Nephrotic syndrome:
• decreased plasma oncotic pressure, ECV is reduced
• Cirrhosis:
• systemic arterial vasodilation leads to ADH release
• Heart failure:
• low cardiac output and reduced systemic blood pressure leads to ADH
release

9. Hyponatremia: hypervolemia
• Renal failure :
• The kidney's ability to excrete a free water load becomes limited as
GFR declines. As a result, patients with advanced renal failure are
at risk for retaining ingested water and developing hyponatremia,
despite suppression of ADH

10. Hyponatremia
hypovolemia
Urine Na
> 20
mmol/L
Diuretics
Ketonuria
RTA
CSW
hypoldosteronism
Urine Na
< 20
mmol/L
GI loose
3rd space
Skin loose
Exercise
normovolemia
Urine
osm?
LOW
Polydipsia
Hypotonic
IVF
Urine
osm?
HIGH
SIADH
hpervolemia
Urine
Na > 20
mmol/L
Acut/chronic
renal failure
Urine Na
< 20
mmol/L
CHF
Chirrhosis
NS

11. Hyponatremia: management
• Fluid restriction in patients with ADH release.
• Administration of oral or intravenous sodium chloride.
• Treatment of the underlying disease

12. Hyponatremia: management
• Rate of correction : depend on
• chronic hyponatremia (>24 hours) , they have cerebral adaption,
which protects them from cerebral edema, but makes them more
susceptible to osmotic demyelination with rapid correction.
• Severe neurologic symptoms with acute hyponatremia. In these
patients, there is no time for cerebral adaption, and a more rapid
approach using hypertonic saline is used for correction.
• Severe hyponatremia : rapid correction can lead to a severe and
sometimes irreversible osmotic demyelination syndrome. Most
reported cases have occurred when the plasma sodium corrections
exceeded 10 mEq/L in a 24-hour period.

13. Hyponatremia: management
• Isotonic vs hypotonic maintenance IV fluids
• These points are illustrated in a systematic review that reported the
use of hypotonic solution as maintenance fluid for hospitalized
children was associated with an increased risk of hyponatremia
(plasma sodium <136 mEq/L) and severe hyponatremia (plasma
sodium <130 mEq/L), which was thought to be due to impaired
ability to excrete free water due to ADH secretion.

14. Hyponatremia: management
Severe CNS symptoms or Na<120 mEq/L
• plasma sodium should be raised until neurologic findings
subside (eg, seizures cease) or the plasma sodium reaches
120 mEq/L
• 3 % hypertonic saline
• mEq sodium infused =
[desired plasma sodium (mEq/L) - actual sodium (mEq/L)] x 0.6 x weight
(kg)
• given slowly, over the course of three to four hours,
aiming not to increase the plasma sodium by more
than 3 mEq/L per hour

15. Hyponatremia: management
Normal or increased ECV
• Water restriction to 60 percent of usual daily
maintenance fluid will allow for the slow correction of
volume imbalance and normalization of plasma sodium as
excess free water is excreted
• Hypotonic fluids should be avoided since any ongoing
ADH secretion will result in more distal tubule free water
reabsorption that will counter the correction of
hyponatremia by fluid restriction

16. Hyponatremia: management
Decreased ECV
• hypervolemic with a decreased ECV due to heart failure,
nephrotic syndrome, or cirrhosis, the treatment choice consists
of treating the underlying conditions, and fluid restriction
• Effective volume depletion due to hypovolemia:
administered fluid will remain in the ECV, it will inhibit activation
of the renin-angiotensin-aldosterone axis and ADH release,
and limit the free water reabsorption.
• In this setting, sodium deficit is a combination of the sodium
loss in the isotonic fluid deficit (each kilogram of body
weight represents one liter deficit of water and 140 mEq loss of
sodium) and the loss of sodium in the remaining current
hyponatremic state, which is calculated as follows:
Hyponatremic sodium deficit = Current total body water (TBW) x
(desired plasma sodium - actual sodium)

17. Hyponatremia : Clinical example
• 10 kg child (desired TBW = 0.6 times body weight) is estimated to have a 10 %
hypovolemic loss and a serum/plasma sodium concentration of 120 mEq/L
• Desired TBW = 6 L
• Total fluid deficit: 10 percent of 10 kg = 1 L
• Current TBW = 5 L
• Sodium (Na) deficit from isotonic fluid deficit = 1 L x 140 mEq/L = 140 mEq
• Hyponatremic sodium deficit = Current TBW x (desired serum Na – current serum Na) = 5 L
x (135 mEq/L – 120mEq/L) = 75 mEq
• Total sodium deficit = 215 mEq
• Child received a 20 mL/kg bolus of normal saline (200 mL of water and 30 mEq Na)
• total fluid needs is 2800 mL (800 mL of remaining fluid deficit, and 2000 mL for two days
of maintenance needs [daily rate of 1000 mL/day]) with total sodium needs of 245 mEq
(185 mEq of the remaining sodium deficit and 60 mEq for two days of maintenance needs
[daily rate of 30 mEq/day
• If there are no ongoing losses, then the half isotonic saline at a rate of 60 mL/hour x 48
hours would best approximate these needs

18. Hypernatremia
• Serum or plasma sodium greater than 150 mEq/L
• True incidence of pediatric hypernatremia is unknown, as
published data are based on hospitalized children.
• Most often caused by the failure to replace water losses,
which, in children, are most commonly due to
gastrointestinal fluid loss

19. Hypernatremia: Etiology
causes of pediatric hypernatremia can be separated into
mechanisms
• Water loss that is not replaced
• Loss of body fluids with a sodium concentration that is less than
serum or plasma sodium will result in an increase in sodium
concentration if the water losses are not replaced. Like
gastrointestinal fluids, dilute urine, and skin loss due to sweat or
burns
• Inadequate water intake that fails to replace ongoing normal fluid
losses
• Excessive salt intake relative to water ingestion
• Iatrogenic administration of excess sodium or salt poisoning

20. Hypernatremia: Etiology
Gastrointestinal loss
• most common cause of hypernatremia is hypotonic gastrointestinal
losses without replacement. GE due to rotavirus can present with
watery diarrhea and hypernatremia.
Skin loss
• normal sweating causes only small free water losses and does not
typically lead to hypernatremia. However, with vigorous or
sustained exercise, or significant febrile illness, water losses from
sweat can become more and can result in hypernatremia if not
corrected with water intake. Increased insensible water losses due
to burns can also lead to hypernatremia

21. Hypernatremia: Etiology
Urinary concentration defects: due to ADH deficiency or
resistance, which leads to excretion of a dilute urine (urine
osmolality less than plasma osmolality) and excessive
urinary free water loss.
Central DI
• Inadequate production or release of ADH.
• Congenital central nervous system (CNS)
malformations , genetic syndromes with associated
CNS anomalies ,CNS tumors, infiltrative processes of
the hypothalamic-pituitary stalk and sequelae from
neurosurgery and trauma.

22. Hypernatremia: Etiology
Nephrogenic DI
• Inadequate renal tubular response to ADH
• Congenital nephrogenic DI
• Mutations in the vasopressin type 2 receptor, X-linked disorder,
present in the first weeks of life with fussiness, low-grade fever, and
polyuria with hypernatremia.
• Acquired nephrogenic DI
• Drug toxicity : Lithium, amphotericin
• Hypercalcemia and hypokalemia
• Renal disease : obstructive uropathy, sickle cell disease,
nephronophthisis, cystinosis, and acute or chronic kidney disease

23. Hypernatremia: Etiology
Osmotic diuresis
urinary water losses due to renal excretion of nonelectrolyte,
nonreabsorbed solutes, such as mannitol or glucose.
Inadequate water intake
• If normal free water losses are not replaced, either because of
lack of access to water , unable to communicate their need for
fluids or lack of thirst.
• Infants and children who are dependent on others for fluid
intake or who have an impaired thirst mechanism are more
vulnerable to hypernatremic hypovolemia.

24. Hypernatremia: Etiology
Excess salt intake
• Iatrogenic causes
Sodium bicarbonate infusions for metabolic acidosis or hypertonic
saline
• Salt poisoning
• Incorrect formula preparation and as an intentional form of child
abuse
• teaspoon of salt contains 100 mEq of sodium , which can increase
the serum sodium concentration in a 10 kg child by 17 mEq/L.
• Salt poisoning causes a rapid onset of hypernatremia, often
resulting in cerebral hemorrhage and irreversible neurologic injury.
Osmotic demyelination can occur, similar to the injury caused by a
rapid elevation in serum sodium in patients with chronic
hyponatremia
• Salt poisoning is associated with weight gain and increased urinary
sodium excretion

25. Hypernatremia
hypovolemia
Urine Na >
20 mmol/L
Osmotic Diuretics
Urine Na <
20 mmol/L
GI loose
Insensible
loose
Poor water
intak
normovolemia
Urine
osm?
LOW
DI
hpervolemia
Urine Na
> 20
mmol/L
Hypertonic
IVF
High Na
intake
Urine Na <
20 mmol/L
hyperaldosteronusm

26. Hypernatremia: management
Emergent fluid resuscitation
• In patients with moderate to severe hypovolemia, fluid
resuscitation with isotonic fluid is administered to restore
intravascular volume and tissue perfusion.
• However, excessive fluid resuscitation needs to be avoided to
prevent volume overload, which may be associated with
cerebral edema.
Calculating the free water deficit
• Free water deficit in liters = Current total body water x ([current
plasma Na/140] - 1)
• Estimate that the 4 mL/kg of free water will lower plasma
sodium by approximately 1mEq/L
• Free water deficit in liters = (4 mL/kg) x (weight in kg) x (desired
change in plasma Na)

27. Hypernatremia: management
Rate of correction
• does not exceed a fall of sodium greater than
0.5 mEq/L per hour (ie, 10 to 12 mEq/L per day)
Treatment of specific etiologies
• in cases where a chronic condition is identified, such as
nephrogenic or central diabetes insipidus, therapy
directed to the underlying condition (eg, administration
of desmopressin) should be initiated in addition to
providing free water replacement.

28. Hypernatremia : Clinical example
• A 10 kg child (TBW 0.6 times body weight) is estimated to have a 10
percent hypovolemic loss (about 1 liter of fluid) and
a serum/plasma sodium concentration of 156 mEq/L.
• Total fluid deficit: 10 percent of 10 kg = 1000 mL
• Free water deficit: 6 L [(156/140 mEq/L) - 1] = 686 mL
• Isotonic loss: Total fluid deficit - water deficit = 314 mL
• Child received a 20 mL/kg bolus of normal saline (200 mL of water
and 30 mEq Na), replacing all but 114 mL of the isotonic fluid loss
• Correction will be over 48 hours
• Total fluid needs is 2800 mL (686 mL of free water deficit, 114 mL of
the isotonic fluid loss and 2000 mL for two days of maintenance
needs [daily rate of 1000 mL/day]) with total sodium needs of 77
mEq (17 mEq for isotonic fluid loss and 60 mEq for two days of
maintenance needs [daily rate of 30 mEq/day]
• In this case, administration of one-quarter isotonic saline at
58 mL/hour for 48 hours would provide adequate replacement of
maintenance needs and remaining isotonic deficit