more sodium is dangerous

1. Dr. Bikal Lamichhane
Internal Medicine
Ist Yr Resident
Hypernatremia

2. Definition
 Hypernatremia is defined as a plasma [Na+] >145 mEq/L and represents a state
of hyperosmolality
Etiology
 Hypernatremia caused by a primary Na+ gain or a water deficit(more common).
 Hyperosmolar state stimulates thirst and the excretion of a maximally
concentrated urine.
 In hypernatremia these compensatory mechanisms are impaired.
 Impaired thirst response may occur in situations where access to water is
limited,often due to physical restrictions (institutionalized, handicapped,
postoperative, orintubated patients) or the mentally impaired (delirium, dementia).

3. Hypernatremia due to water loss.
Nonrenal water loss may be due to evaporation from the skin and respiratory tract
(insensible losses) or loss from the GI tract.
 Diarrhea is the most common GI cause of hypernatremia.
 Osmotic diarrhea (induced by lactulose, sorbitol, or malabsorption of carbohydrate) and
viral gastroenteritis result in disproportional water loss.
Renal water loss results from either osmotic diuresis or diabetes insipidus
Osmotic diuresis is frequently associated with glycosuria.
 Increased urea generation from accelerated catabolism, high protein feeds, and stress-
dose steroids can also result in an osmotic diuresis.

4. Hypernatremia secondary to nonosmotic urinary water loss is caused by
(a) impaired vasopressin secretion (central diabetes insipidus [CDI]) or
(b) resistance to the actions of vasopressin (nephrogenic diabetes insipidus
[NDI]).
Cause of CDI is destruction of the neurohypophysis from trauma, neurosurgery,
granulomatous disease, neoplasms, vascular accidents, or infection.
NDI may either be inherited or acquired.
 Disruption to the renal concentrating mechanism due to drugs
(lithium,demeclocycline, amphotericin), electrolyte disorders (hypercalcemia,
hypokalemia),medullary washout (loop diuretics), and intrinsic renal diseases.

5.  Hypernatremia due to primary Na+ gain can rarely occur after repetitive
hypertonic saline administration or chronic mineralocorticoid excess.
 Transcellular water shift from ECF to ICF can occur in circumstances of
transient intracellular hyperosmolality, as in seizures or rhabdomyolysis

6. DIAGNOSIS
Clinical Presentation
 Hypernatremia results in contraction of brain cells as water shifts to attenuate the
rising ECF osmolality.
 Symptoms includes altered mental status, weakness, neuromuscular
irritability,focal neurologic deficits, and, occasionally, coma or seizures.
 Chronic hypernatremia is generally less symptomatic as a result of adaptive
mechanisms designed to defend cell volume.
 CDI and NDI generally present with complaints of polyuria and thirst. Signs of
volume depletion or neurologic dysfunction are generally absent unless the patient
has an associated thirst abnormality.

7. DIAGNOSTIC TESTING
Laboratories
 Urine osmolality and the response to desmopressin acetate (DDAVP) narrow the differential
diagnosis for hypernatremia.
 The appropriate renal response is a small volume of concentrated (urine osmolality >800 mOsm/L)
urine.
 Submaximal urine osmolality (<800 mOsm/L) suggests a defect in renal water conservation.
 A urine osmolality <300 mOsm/L in the setting of hypernatremia suggests complete forms of CDI
and NDI.

8.  Urine osmolality between 300 and 800 mOsm/L can occur from partial formsof
diabetes insipidus (DI) as well as osmotic diuresis.
 The two can be differentiated by quantifying the daily solute excretion.
 A daily solute excretion >900 mOsm/L defines an osmotic diuresis.
 Response to DDAVP. Complete forms of CDI and NDI can be distinguished by
administering the vasopressin analog DDAVP (10 mcg intranasally) after careful
water restriction.
 The urine osmolality should increase by at least 50% in complete DI and does not
change in NDI.

10. TREATMENT
 Aggressive correction of hypernatremia is potentially dangerous. The rapid shift of water
into brain cells increases the risk of seizures or permanent neurologic damage.
 Therefore, the water deficit should be reduced gradually by roughly 10 to 12 mEq/L/d.
 In chronic asymptomatic hypernatremia, due to the cerebral adaptation to the chronic
hyperosmolar state, the plasma [Na+] should be lowered at a more moderate rate
(between 5 and 8 mEq/L/d).

11. Intervention
 The mainstay of management is the administration of water, preferably by mouth
or nasogastric tube.
 Alternatively, 5% dextrose in water (D5W) or quarter NS can be given i/v.
 Traditionally, correction of hypernatremia has been accomplished by calculating
free water deficit by the equation:
 Free water deficit = {([Na+] -140)/140} x (TBW)

12.  Specific therapies for the underlying cause:-
 Hypovolemic hypernatremia
 In patients with mild volume depletion,Na+-containing solutions, such as 0.45%
NS, can be used to replenish the ECF as well as the water deficit.
 If patients have severe or symptomatic volume depletion, correction of volume
status with isotonic fluid should take precedence over correction of the
hyperosmolar state.
 Once the patient is hemodynamicallystable, administration of hypotonic fluid can
be given to replace the free water deficit.
Hypernatremia from primary Na+ gain is unusual.
 Cessation of iatrogenic Na+ is typically sufficient.

13. DI with hypernatremia. DI is best treated by removing the underlying cause.
CDI. Because the polyuria is the result of impaired secretion of vasopressin,
treatment is best accomplished with the administration of DDAVP, a vasopressin
analog.
NDI. A low-Na+ diet combined with thiazide diuretics will decrease polyuria
through inducing mild volume depletion. This enhances proximal reabsorption
of salt and water, thus decreasing urinary free water loss. Decreasing protein
intake will further decrease urine output by minimizing the solute load that
must be excreted.