ELECTROLYTE

IMBALANCE :
SODIUM

Submitted by:

Milosantos, john francis d.

Tuibeo, Ma. Arlyn P.

Yu, Aldrin Anthony l.

Submitted to:

Mr. Darwin aznar

Sodium:

Sodium is the most abundant electrolyte in the ECF; its concentration ranges from 135 to 145 mEq/L
(135 to 145 mmol/L) and it is the primary determinant of ECF volume and osmolality. Sodium has a
major role in controlling water distribution throughout the body, because it does not easily cross the cell
wall membrane and because of its abundance and high concentration in the body. Sodium is regulated
by ADH, thirst, and the rennin-angiotensin-aldosterone system.

Sodium also functions in establishing the electrochemical state necessary for muscle contraction and the
transmission of nerve impulses. Syndrome of inappropriate secretion of antidiurectic hormone (SIADH).
Decrease in the circulating plasma osmolality, blood volume, or blood pressure, arginine vasopressin
(AVP) is released from the posterior pituitary. Oversecretion of AVP can cause SIADH. Patients who are
at risk are the elderly, those on mechanical ventilation, and people taking selective serotonin reuptake
inhibitors.

Sodium imbalance can develop under simple or complex circumstances. The two most common sodium
imbalances are sodium deficit and sodium excess.

Sodium Deficit (Hyponatremia):

Hyponatremia refers to a serium sodium level that is less than 135 mEq/L. plasma sodium concentration
represents the ratio of total body sodium to total body water, Decrease in this ration can occur because
of low total body sodium with a lesser reduction in total body water. Hyponatremic state can be
superimposed on an existing FVD or FVE.

2 types of sodium imbalance:

Sodium deficit (hyponatremia) S/S:

- Anorexia, nausea and vomiting, headache, lethargy, dizziness, confusion, muscle cramps and
weakness, muscular twitching, seizures, papilladema, dry skin, pulse, BP, weight gain,
edema.

Labs indicate:

- Serum sodium and urine sodium, urine specific gravity and osmolality.

Sodium Excess (hypernatremia) S/S:

- Thirst, elevated body temperature, swollen dry tongue and sticky mucous membranes,
hallucinations, lethargy, restlessness, irritability, focal or grand mal seizures, pulmonary edema,
hyperreflexia, twitching, nausea, vomiting, anorexia, pulse, and BP.

Labs Indicate

- Serum sodium, urine sodium, urine specific gravity and osmolality, CVP.

Clinical Manifestations:

Depend on the cause, magnitude, and speed with which the deficit occurs. Poor skin turgor, dry mucosa,
headache, decreased saliva production, orthostatic fall in blood pressure, nausea, vomiting, and
abdominal cramping occur. Neurologic changes, altered mental status, status epilepticus, and coma.
Related to the cellular swelling, and cerebral edema associated with hyponatremia.

Patients with an acute decreased in serum sodium levels have more cerebral edema and higher
mortality rates than do those with more slowly developing hyponatremia. Developing in less than 48
hours, associated with brain herniation and compression of midbrain structures. Chronic decreases in
sodium, developing over 48 hours or more, can occur in status epilepticus and cerebral pontine
myelinolysis.

Features of hyponatremia associated with sodium loss and water gain include anorexia, muscle cramps,
and a feeling of exhaustion. The severity of symptoms increases with the degree of hyponatremia and
the speed with which it develops. When the serum sodium level decreases to less than 115 mEq/L (115
mmol/L), signs of increasing intracranial pressure, such as lethargy, confusion, muscle twitching, focal
weakness, hempiparesis, papilledema, seizure, and death, may occur.

Medical Management:

The key to treating hyponatremia is assessment including identifying patients who are at risk and
recognizing that the rapidity of the onset of hyponatremia is of primary importance.

Sodium Replancement:

The most common treatment for hyponatremia is careful administration of sodium by mouth,
nasogastric tube, or a parenteral route. For patients who can eat and drink, sodium is easily replaced.
Sodium is consumed abundantly in a normal diet. Lactated ringer’s solution or isotonic saline solution
may be prescribed. Serum sodium must not be increased more than 12mEq/L in 24 hours to avoid
neurologic damage due to osmotic demyelination. This condition may occur when the serum sodium
concentration is overcorrected too rapidly or in the presence of hypoxia or anoxia. It may produce
lesions that show symmetric myelin destruction affecting all the fiber tracts that cause paraparesis ,
dysarthria, dysphagia, and coma.

Excess sodium would be excreted rapidly in highly concentrated urine. With the addition of the diuretic
furosemide (Lasix).

Water Restriction:

A patient with normal or excess fluid volume, hyponatremia is treated by restricting fluid to a total of
800 ml in 24 hours. This is far safer than sodium administration and is usually unaffective treatment.
Symptoms are severe (seizures delirium coma) as well as in traumatic brain injury, it maybe necessary to
administer small volume of hypertonic sodium solution. In correct used of these fluids is extremely
dangerous because one liter of 3% sodium chloride solution contains 513 mEq of sodium and 1 liter of
5% sodium chloride solution contains 855 mEq of sodium.

If edema exists alone, sodium is restricted; if edema and hyponatremia occur together, both sodium and
water is restricted.

Nursing Management:

- Identify and monitor patients at risk of hyponatremia to prevent serious consequences

- Monitor fluid I & 0
- body weight must be alert for central nervous system changes
 - encourage foods and fluids with high sodium content
- the nurse also be familiar of the sodium content of parenteral fluids

Clinical Manifestation:

Changes maybe manifested by restlessness and weakness in moderate hypernatremia and by

disorientation, delution, and hallucination in severe hypernatremia

- dehydration

Primary characteristic:

Thirst is such a strong defender of serum in healthy people that hypernatremia never unless the person
is unconscious or does not have water. Other signs:

D dry skin
D swollen tongue
D sticky mucous membrane
D flushed skin
D peripheral and pulmonary edema
D postural hypertension
D oliguria
D increased muscle tone
D deep tendon reflexes
D

Assessment and Diagnosis findings:

The serum sodium level exceeds 145 mEq/L (145 mmol/L). Patients with nephrogenic or central diabetes
insipidus have hypernatremia and produce a dilute urine with a urine osmoliality less than 250
mOsm/kg.

Medical Management:

Consists of a gradual lowering of the serum sodium level by the infusion of a hypotonic electrolyte
sodium (sodium choride) or an isotonic nonsaline solution (D5W). water needs to be replaced without
sodium. Clinicians consider a hypotonic sodium solution to be safer the D5W because it allows a gradual
reduction in the serum sodium level, thereby decreasing the risk of cerebral edema. Solution of choice in
severe hyperglycemia with hypernatremia. Serum sodium level temporarily decreases the plasma
osmolality below that of the fluid in the brain tissue, causing dangerous cerebral edema. Diuretics also
may be prescribed to treat the sodium gain.

No consensus about the exact rate at which serum sodium levels should be reduced. The serum sodium
level is reduced at a rate no faster than 0.5 to 1 mEq/L/h to allow sufficient time for readjustment
through diffusion across fluid compartments.
Nursing Management:

Fluid losses and gains are carefully monitored in patients who are at risk for hypernatremia. The nurse
should assess for abnormal losses of water or low water intake and for large gains of sodium.

Obtains a medication history, because some prescription medications have a high sodium content. The
nurse also notes the patient’s thirst or elevated body temperature and evaluates it in relation to other
clinical signs. The nurse monitors for changes in behavior, such as restlessness, disorientation, and
lethargy.