Nznanskssk

1. HYPERNATREMIA

2. • Hypernatremia is defined as a Plasma Na+ that is greater than 145
mmol/L.
• Hypernatremia is not a final diagnosis; rather it is a laboratory finding that
occurs in other disorders.
• Although the concentration of Na+ is a ratio of Na+ to water in the ECF
compartment, in majority of patients, hypernatremia is primarily due
to a deficit of water.
• This almost means that ICF volume is contracted.

3. Understand ‘Link between Na and Water’
• Baseline Na 140 mmol/L [ L – Water is the denominator !!]
• 10% decrease in plasma water – Increases Na to 154 mmol/L [+14]
• 10% Increase in plasma water – Decreases Na to 126 mmol/L [-14]
• Volume Preservation is the primary target in Water Homeostasis
• Maintaining Na 135 -145 mmol/L [Osmolality] is the secondary target
• When there are conflicting signals, Volume Preservation is the priority

4. Gain of Na+
(positive Na+ balance)
Loss of water
(negative water balance)

5. PRIMARY WATER DEFICIT
REDUCED WATER INTAKE FOR
MANY DAYS
• Lack of water
• Inability to gain access to, or to
drink water
• Defective thirst:
 Altered mental state
 Psychological disorder
 Diseases involving the
osmoreceptors
 Diseases involving thirst centre
INCREASED WATER LOSS
• Renal loss:
 Diabetes insipidus (CDI/NDI)
 Osmotic diuresis
 Release of vasopressinase
• GI loss:
 Vomiting
 Osmotic diarrhoea
• Cutaneous loss:
 Excessive sweating
• Respiratory loss:
 hyperventilation

6. PRIMARY WATER DEFICIT
REDUCED WATER INTAKE FOR
MANY DAYS
• Lack of water
• Inability to gain access to, or to
drink water
• Defective thirst:
 Altered mental state
 Psychological disorder
 Diseases involving the
osmoreceptors
 Diseases involving thirst centre
INCREASED WATER LOSS
• Renal loss:
 Diabetes insipidus (CDI/NDI)
 Osmotic diuresis
 Release of vasopressinase
• GI loss:
 Vomiting
 Osmotic diarrhoea
• Cutaneous loss:
 Excessive sweating
• Respiratory loss:
 hyperventilation
DEHYDRATION vs HYPOVOLEMIA

7. PRIMARY WATER DEFICIT
REDUCED WATER INTAKE FOR MANY
DAYS
• Lack of water
• Inability to gain access to, or to drink water
• Defective thirst:
 Altered mental state
 Psychological disorder
 Diseases involving the osmoreceptors
 Diseases involving thirst centre
INCREASED WATER LOSS
• Renal loss:
 Diabetes insipidus (CDI/NDI)
 Osmotic diuresis
 Release of vasopressinase
• GI loss:
 Vomiting
 Osmotic diarrhoea
• Cutaneous loss:
 Excessive sweating
• Respiratory loss:
 hyperventilation
SHIFT OF WATER INTO CELLS:
• Gain of “effective” osmoles in the ICF compartment (seizures, rhabdomyolysis)

8. PRIMARY GAIN OF Na+
• Administration of intravenous saline with a higher concentration of
Na+ & K+ than their concentration in the urine during an osmotic or a
water diuresis.
• Infusion of hypertonic NaCl or NaHCO3 in oliguric patient.
• Ingestion of sea water or replacing sugar by NaCl in feeding formula
in infants

10. RESPONSE TO HYPERNATREMIA
(when the P Na+ rises, water control system elicits two responses that are
designed to lower the P Na+ to prevent a further decrease in brain cell size)
Stimulation
of thirst
Water
reabsorption in
kidneys
• It is virtually impossible to have the P Na+
increase above the normal range if the thirst
response is intact and water is available.
• In patients with significant hypernatremia, look
for a reason why they cannot appreciate thirst or
gain access of water.
• If vasopressin is not present or if it fails to act.
• Water diuresis ensues.
• Resultant increased URINE FLOW RATE & decreased
URINE OSMOLALITY.

11. WHEN VASOPRESSIN ACTS
WHEN VASOPRESSIN IS
NOT THERE OR CANNOT
ACT

12. ACUTE
HYPERNATREMIA
• rapid increase in plasma Na+. (48 hours)
• Decrease in the size of cells in the body.
• Organ most affected is the brain.
• As brain volume declines, vessel coming from the inner
surface of skull become stretched, and thus are at risk
for rupture.

13. ACUTE
HYPERNATREMIA
• rapid increase in plasma Na+. (48 hours)
• Decrease in the size of cells in the body.
• Organ most affected is the brain.
• As brain volume declines, vessel coming from the inner
surface of skull become stretched, and thus are at risk
for rupture.
CHRONIC
HYPERNATREMIA
• Slowly developing hyponatremia or long standing.
• Cells in brain gain effective osmoles, and this returns
their volume back to normal.
• Whilst, if seum Na+ is rapidly lowered, causes brain
cells to swell, as they cannot lose these extra newly
gained osmoles quickly.
• May lead to cerebral edema, herniation.

14. Gain of Na+
(positive Na+ balance)
Loss of water
(negative water balance)

15. SKIN LOSSES
• As both insensible (transdermal by diffusion) and sensible (sweat loss).
• Under normal conditions, sweat volume is 500 – 700 mL/day.
• Sweat losses may be dramatically high during fever, exercises and exposure to
high temperature.
• Sweat is hypotonic to plasma.
• Excessive sweating promotes free water loss, leading to rise in serum Na+.
EXCESSIVE SWEATING + INADEQUATE WATER INTAKE HYPERNATREMIA
EXCESSIVE SWEATING + EXCESSIVE WATER INTAKE HYPONATREMIA

16. GI LOSSES
• Both upper and lower GI losses can result in hypernatremia when water
intake is limited.
• Loss of both gastric secretions (vomiting or drainage), and small
intestinal secretions have sodium level well below that in the plasma,
therefore promote development of hypernatremia
OSMOTIC DIARRHEA HYPERNATREMIA
SECRETORY DIARRHEA HYPONATREMIA

17. URINARY LOSSES
DIABETES INSIPIDUS OSMOTIC DIURESIS
• Decreased release (central) or
• renal resistance (nephrogenic)
• Most patients with DI have a normal thirst
mechanism
• They typically present with polyuria, polydipsia,
and a high-normal serum Na+.
• Is thirst gets affected in DI, they can have
marked and symptomatic hypernatremia.
 Lesions involving thirst center.
 Infants & young children
 Postoperative period
 Older patients
• Nonreabsorbed, nonelectrolyte solutes
• Glucose, mannitol, or urea.
• Among these 3
• Glucose and mannitol can cause both hypo
as well as hypernatremia.
• But urea produces only hypernatremia as
it is an ineffective osmole.

18. HYPOTHALAMIC LESIONS AFFECTING THIRST OR
OSMORECEPTOR FUNCTION
• Hypernatremia can occur in the absence of increased water losses if there is
primary hypothalamic disease impairing the thirst…….. (hypodipsia)
• A defect in thirst with or without concomitant DI can be seen in children
with either congenital or acquired hypothalamic structural lesions.
• As an example: infants with holoprocencephaly (dysplasia of the brain
midline structures) may show no signs of thirst even when their serum
osmolality exceeds 330 mosm/kg.
• In such patients, forced water intake is usually sufficient to maintain the
normal serum sodium, although central diabetes insipidus, if present, must
also be treated.

19. ADIPSIC DIABETES INSIPIDUS
• Earlier called as ESSENTIAL HYPERNATREMIA. ( central DI with deficient thirst)
• Occurs when both ADH secretion & Thirst are impaired.
• Affected patients are vulnerable to recurrent episodes of hypernatremia.
• Patients typically have moderate to severe hyponatremia with serum Na+ ranging 155 – 190.
• Most patients may be asymptomatic due to chronicity.
• Causes: congenital or acquired central nervous system lesions.
• M/C – septo-optic dysplasia, germinoma, rupture or clipping of ACA of COW, CNS sarcoidosis.
• Can be accompanied by autoantibodies to Na(x) channel , sodium sensing receptor in hypothalamus. Young
patients with hypernatremia, no thirst and no vasopressin response.

20. Gain of Na+
(positive Na+ balance)
Loss of water
(negative water balance)

21. SODIUM OVERLOAD
• Can be acute and marked sometimes.
• Induced by the administration of hypertonic sodium solutions.
• Examples:
1. Accidental or nonaccidental salt poisoning in infants and young children.
2. Hypertonic NaHCO3 in treatment of metabolic acidosis.
3. Hypertonic saline in traumatic head injury.
4. Hypertonic saline irrigation of hydatid cysts.
5. Systemic absorption of hypertonic saline administered into uterus to induce
abortion.
6. Massive salt ingestion.

22. SALT POISONING
• Infrequent problem that primarily occurs in infants and young children but has
been reported in adults.
1. Surreptitious intentional salt poisoning as a form of child abuse. A tablespoon
of salt contains 100mEq of Na, which can increase the serum Na+ by 10mEq in
10kg child.
2. The accidental substitution of salt for sugar in infant formula.
3. In some parts of world, the custom of “salting” of newborns by grandparents.

23. MANIFESTATIONS OF ACUTE HYPERNATREMIA
• Rapid decrease in brain volume can cause rupture of brain vessels , leading to
intracerebral and subarachnoid hemorrhages and possible irreversible neurological
damage.
• Can also cause demyelinating lesions similar to ODS.
• May begin with lethargy, weakness, and irritability, and can progress to twitching,
seizures and coma.
• Severe symptoms is serum Na+ is > 158 mEq/L.
• Serum Na+ > 180 are associated with high mortality, especially in adults.

24. MANIFESTATIONS OF CHRONIC HYPERNATREMIA
• HYPERNATREMIA that has been there for more than a day.
• Less likely to present neurological symptoms because of cellular adaptation.
• Even if present, symptoms are difficult to distinguish from underlying neurological
condition.
• Overall increased mortality and morbidity.
• RAPID CORRECTION OF HYPERNATREMIA:
 In infants, correction must occur slowly (less than 10-12 mEq/day)
 In adults, rapid correction has not been shown to have adverse consequences. Risk of
cerebral edema is less, although adults are always undertreated.

25. Diagnostic
evaluation of
hypernatremia

26. The cause of hypernatremia is usually evident from the history.
In adults, it is most often due to water losses in older patients whose
losses are not replaced because of impaired mental status.
On the other hand, a hypothalamic lesion affecting the thirst center
should be strongly suspected in an alert patient with access to water
who has serum Na+ concentration above 150 mEq/L.

27. INVESTIGATIONS
1. Serum osmolality
2. Urine osmolality
3. Kidney function test
4. Urinary electrolyte measurement
5. Response of urinary osmolality to ADH administration
6. Water deprivation test
7. Plasma ADH measurement

28. NORMAL RESPONSE
RISE IN SERUM SODIUM
RISE IN PLASMA
OSMOLALITY
STIMULATION OF THIRST
&
ADH RELEASE
INCREASED
REABSORPTION OF
FREE WATER
URINARY CONCENTRATION
LEADING TO INCREASED
URINARY OSMOLALITY

29. THERFORE,
IF BOTH HYPOTHALAMIC AND RENAL FUNCTIONS ARE INTACT
IN PRESENCE OF HYPERNATREMIA
URINE OSMOLALITY SHOULD BE ABOVE 600 mOsm/kg
(if given, exogenous ADH should not produce a further rise in the urine
osmolality)

30. IF URINE OSMOLALITY IS LOW (<300 mOsm/kg)
(urine osmolality less than plasma osmolality)
Patient has either central or nephrogenic DI
(high urine output with low urine osmolality)
RESPONSE TO EXOGENOUS
dDAVP administration
Nephrogenic
diabetes
insipidus
Central
diabetes
insipidus

31. IF URINE OSMOLALITY IS INTERMEDIATE
(300 – 600 mOsm/kg)
OSMOTIC DIURESIS DIABETES INSIPIDUS
• Can be confirmed by measuring urine total solute
excretion. ( product of urine osmolality and UO)
• If more than 1000 mOsm/day its s/o presence of an
osmotically active substance (normal 600 – 900).
• Does not respond to exogenous ADH.

32. IF URINE OSMOLALITY IS HIGH
(>600 mOsm/kg)
MOST LIKELY REASON IS EXTRA-
RENAL FLUID LOSS
POSSIBILITY OF
PARTIAL DIABETES
INPIDIUS

33. TREATMENT OF
HYPERNATREMIA IN
ADULTS

34. • Correction of hypernatremia requires the administration of dilute
fluids to correct the water deficit and replace the ongoing loss.
• Patients with hypernatremia usually have a serious underlying
conditions, so such patients usually requires hospitalisations.
• In general, a net positive balance of 3 mL of electrolyte free water
per Kg of lean body weight will lower the serum sodium by
approximately 1 mEq/L.

35. PATIENTS WITH CHRONIC HYPERNATREMIA
• D5W, intravenously @ 1.35 mL/hour/kg of weight, up to maximum of 150 mL/hour.
• Approx, 70 mL/hour in 50 kg patient, and 100 mL/hour in 70 kg patient.
• If patient is clinically stable ( level of sensorium is normal, and can drink water orally ),
hyponatremia can also be corrected using oral rehydration, or administering water
through nasogastric tube.
The goal of correction is to lower the serum sodium by
approximately 10 mEq/L in 24 hours and not more than
12 mEq/L in 24 hours.

36. PATIENTS WITH ACUTE HYPERNATREMIA
• D5W, intravenously, @ 3 to 6 mL/kg/hour, up to a maximum of 666 mL/hour.
• The serum Na+ and BG to be monitored every hourly, till serum Na+ is lowered below 145.
• Once the serum Na+ is lowered below 145, the rate of infusion is reduced to 1
mL/kg/hour.
• Goal is to lower the serum sodium by 1-2 mEq/L per hour and to restore a normal serum
Na+ in less than 24 hour.
• Patients with central diabetes insipidus requires desmopressin therapy.
• Monitor for hyperglycemia

37. RATIONALE FOR THERAPEUTIC APPROACH
ESTIMATE THE
FREE WATER
DEFICIT
DETERMINE
THE RATE OF
CORRECTION
CALCULATE
THE FLUID
REGIMEN
ADDRESS
CONCURRENT
VOLUME &
POTTAISSIUM
DEFICITS

38. ESTIMATING TOTAL WATER DEFICIT

40. DETERMINE THE RATE OF CORRECTION
ACUTE HYPERNATREMIA:-
• Serum sodium should be lowered rapidly to a near normal level in
less than 24 hours.
• Can be treated with iv dextrose or hemodialysis/CVVHF
CHRONIC HYPERNATREMIA:-
• Safe rate to practice is to lower the sodium by less than 12 mEq/day

41. DESIGNING THE FLUID REPLACEMENT REGIMEN
ACUTE HYPONATREMIA:-
• The entire deficit is corrected within 24 hours.
• Hourly infusion rate should exceed the water deficit divided by 24
water deficit calculated (mL)
• Hourly infusion rate (ml/hour) =
24 hours

42. CHRONIC HYPERNATREMIA:
• Only a fraction of total water deficit is replaced in 24 hours
• ie, enough water to lower the serum sodium by 10mEq/L
• Desired water replacement in the first day in mL = 3 mL/kg x 10
Hourly infusion rate =
(mL//kg)
Desired water replacement in the first day in mL
24 hours

43. CALCULATE OR ESTIMATE ONGOING ELECTROLYTE-FREE
WATER LOSSES
• Ongoing free water losses can be estimated or calculated based upon
the volume of the fluid being lost.
• Ongoing urinary free water loss can be calculated from the following
equation
• Urinary free water loss = UV x (1 – {(Una + Uk)/ Sna)}

48. • Excessive salt intake or
iatrogenic fluid
administration.
• Key feature: high urine
osmolality
• Volume status: hypervolemia

49. • Normal water loss from
urine, GIT or sweat which
goes unreplaced
• Key feature : high urine
osmolality.
• Volume status : euvolemia.

50. • Excessive water
loss
1. Extrarenal water
loss
2. Abnormal renal
water loss