HYPONATREMIA AND HYPERNATREMIA

SAMIR EL ANSARY

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•Why is sodium balance critical

to volume control?

Sodium and its corresponding anions

represent almost all of the osmotically

active solutes in the extracellular fluid

under normal conditions.

Therefore the serum

concentration of sodium reflects

the tonicity of body fluids.

Small changes in osmolality are

counteracted by thirst regulation,

antidiuretic hormone (ADH) secretion, and

renal concentrating or diluting

mechanisms.

Preservation of normal serum osmolality

(i.e., 285-295 mOsm/L) guarantees

cellular integrity by regulating net

movement of water across cellular

membranes.

ADH

Its mechanism of action

•ADH is also called arginine vasopressin or

simply vasopressin.

•ADH is a small peptide hormone

produced by the hypothalamus that binds

to the vasopressin 1 and 2 receptors

(V1 and V2).

•Vasopressin release is regulated by

osmoreceptors in the hypothalamus, which

are sensitive to changes in plasma osmolality

of as little as 1 % to 2%.

•Under hyperosmolar conditions,

osmoreceptor stimulation leads to stimulation

of thirst and vasopressin release.

These two mechanisms result in increased

water intake and retention, respectively.

•Vasopressin release is also regulated by

baroreceptors in the carotid sinus and aortic

arch; under conditions of hypovolemia, these

receptors stimulate vasopressin release to

increase water retention by the kidney.

•At very high concentrations,

vasopressin also causes vascular

smooth muscle constriction through the

V1 receptor, increasing vascular tone

and therefore the blood pressure.

Accordingly, vasopressin is often

administered parenterally as a

vasopressor agent in patients with

hypotension that is refractory to volume

resuscitation.

•Does hyponatremia simply mean

there is too little sodium in the

body?

No. The serum sodium

concentration is not a reflection of

the total body sodium content;

instead,it is more representative

of changes in the total body water.

With hyponatremia, defined as serum sodium

level less than 135 mEq/L, there is too much

total body water relative to the amount of total

body sodium, thereby lowering its

concentration.

Despite this key observation, the serum sodium

concentration is not a reflection of volume

status, and it is possible for hyponatremia to

develop in states of volume depletion,

euvolemia, and volume excess.

Assessing a patient's volume status is therefore

the key step in identifying the underlying cause

of hyponatremia .

it is possible for hyponatremia to

develop in states of volume depletion,

euvolemia, and volume excess.

Helpful physical findings include

tachycardia, dry mucous membranes,

orthostatic hypotension, increased skin

turgor (associated with hypovolemia) or

edema, an S3 gallop, jugular venous

distention, and ascites

(present in hypervolemic states).

•Are hyponatremia and

hypoosmolality synonymous?

No. Hyponatremia can occur

without a change in total body

sodium or total body water in two

settings.

The first is pseudohyponatremia, which is a

laboratory artifact in patients with severe

hyperlipidemia or hyperproteinemia.

This laboratory abnormality has been essentially

eliminated by the use of ion-specific electrodes

(rather than flame photometry) to determine the

serum

sodium concentration.

substances (such as glucose or

mannitol) cause hyponatremia but not

hypoosmolality, a condition known as

translocational hyponatremia.

In such states, water is drawn out of cells

into the extracellular space, diluting the

plasma solutes and equilibrating osmolar

differences.

In addition, use of large quantities

of irrigant solutions that do not

contain sodium

(but instead contain

Glycine, sorbitol, or mannitol)

During gynecologic or urologic

surgeries can also cause severe

hyponatremia.

Hyponatremia in a patient with

hypovolemia

Hypovolemic hyponatremia represents a

decrease in total body sodium in excess of

a decrease in total body water.

Simultaneous sodium and water loss can

be due to renal

(such as diuretic use) or extrarenal causes.

Hypovolemia results in a decrease in renal

perfusion, a decrement in the glomerular filtration

rate, and an increase in proximal tubule

reabsorption of

sodium and water; all three mechanisms

contribute to decreased water excretion.

Furthermore, hypovolemia supersedes the

expected inhibition of vasopressin release by

hypoosmolality and maintains the secretion of the

hormone.

The body protects volume at the

expense of osmolality.

HypovolemiaSupersedes the expected

inhibition of vasopressin release

by hypoosmolality

And maintains the secretion of

the hormone.

The body protects

volume

At the expense of

osmolality.

How does hypervolemic

hyponatremia differ from

hypovolemic

hyponatremia?

In hypervolemic hyponatremia, the kidneys are

at the center of the problem because of either

intrinsic renal disease or the renal response to

extrarenal pathophysiology.

Physical examination reveals edema and no

evidence of volume depletion.

Intrinsic renal disease with a compromised

glomerular filtration rate (acute or chronic)

prevents adequate excretion of sodium and

water.

Intake of sodium in excess of

what can be excreted leads to

hypervolemia (edema)

whereas excessive intake of

water leads to hyponatremia.

In contrast, in congestive heart

failure, hepatic cirrhosis, and

nephrotic syndrome, the intrinsically

normal kidney is stimulated to

retain sodium and water in response

to perceived decrements in

intravascular volume and renal

perfusion; as a result, hypervolemia

and hyponatremia develop.

In general, hypervolemic hyponatremia

due to an extrarenal cause is

characterized by a low urine sodium

concentration (<10 - 20 mEq/L)

This distinguishes it from hypervolemic

hyponatremia due to intrinsic renal

causes, where the urine sodium is > 20

mEq/L

{ In renal causes ,kidney can not

re-absorb Na } .

Syndrome of inappropriate

secretion of antidiuretic

hormone (SIADH)

SIADH is a common cause of

euvolemic hyponatremia

SIADH

And is associated with

malignancies, pulmonary disease,

central nervous system disorders,

pain, nausea, and many drugs.

SIADH

Common offending medications include

hypoglycemic agents, psychotropics

(including antipsychotics and

antidepressants), narcotics, and chemo-

therapeutic agents.

Other causes of euvolemic hyponatremia

include psychogenic polydipsia, a low-solute

diet (beer potomania or the tea and toast

diet), hypothyroidism, and adrenal

insufficiency.

Diagnostic tests

useful in the evaluation of

hyponatremia

The physical examination is critical to the

determination of volume status, as previously

described.

Serum electrolyte and serum and urine

osmolality measurements are useful.

High urine osmolality despite low serum

osmolality suggests either hypovolemic

hyponatremia or SIADH if the patient is in

a euvolemic state.

Very low urine osmolality suggests

excessive water intake, as in

psychogenic polydipsia or a low-solute

diet.

Measurements of thyroid stimulating

hormone and cortisol can be used to

assess endocrine causes of

hyponatremia.

In renal causes ,kidney can not

re-absorb Na

The urine sodium concentration can

help distinguish renal and

extrarenal causes of hypervolemic

hyponatremia.

Patients with diabetic ketoacidosis

frequently have hyponatremia

Diabetic ketoacidosis is an example of

hyperosmotic hyponatremia.

In general, serum sodium decreases by

approximately 2.4 mEq/L for every

increase of 100 mg/dL over normal

glucose levels.

In this setting, the serum sodium

level should not be interpreted

without an accompanying

serum glucose measurement, and

the appropriate correction should

be made if the glucose

exceeds 200 mg/dL.

Difference between acute

and chronic

hyponatremia

Acute hyponatremia

A distinct entity in terms of morbidity,

mortality, and treatment strategies.

Most commonly occurs in the hospital

(frequently in the postoperative

setting)

In psychogenic polydipsia, and in

elderly women taking thiazide diuretic

agents.

Chronic hyponatremia

Hyponatremia lasting longer than

48 hours.

The majority of patients who are seen

by physicians or emergency

departments with hyponatremia should

be assumed to have chronic

hyponatremia.

Signs and symptoms of

hyponatremia

Majority of patients have no

symptoms

symptoms

often develop in patients with a

serum sodium concentration

< I25 mEq/L or in whom the

sodium has decreased rapidly.

Gastrointestinal symptoms of nausea,

vomiting, and anorexia occur early

But neuropsychiatric symptoms such as

lethargy, confusion, agitation, psychosis,

seizure, and coma are more common.

Clinical symptoms roughly correlate

with the amount and rate of

decrease in serum sodium levels.

Drugsassociated with hyponatremia

Thiazide diureticsfrequently cause hyponatremia by promoting

sodium excretion in excess of water.

Of note, because loop diuretics directly impair

the creation and maintenance of the medullary

osmotic gradient, they are far less likely to cause

hyponatremia, as little stimulus for water

reabsorption occurs as urine passes through the

collecting duct.

Selective serotonin reuptake inhibitors

and several chemotherapeutic agentscause hyponatremia, and this is thought to occur

through the inappropriate release of ADH.

Nonsteroidal anti-inflammatory drugs block

the production of renal prostaglandins and allow

vasopressin to act unopposed in the kidney,

which

can lead to water retention.

Tricyclic antidepressants and a number

of anticonvulsants are also

associated with hyponatremia.

Last, use of { 3,4-methylene-dioxy-

meth-amphetamine, or Ectasy } ,

particularly in combination with

consumption of large volumes of water, is

associated with severe, life-threatening

hyponatremia.

Therapy for

Hyponatremia

Not all patients with hyponatremia should be

treated alike.

Duration (acute vs. chronic) and the presence or

absence of neurologic symptoms are the most

critical factors in determining the therapeutic

strategy.

The prescribed therapy must take into

consideration the patient's current

symptoms and the risk of provoking a

demyelinating syndrome with

overly rapid correction.

The first priority is circulatory

stabilization with normal saline

solution in patients with significant

volume depletion.

In patients with acute symptomatic

hyponatremia, the risks of delaying treatment,

which could lead to cerebral edema, subsequent

seizures, and respiratory arrest, clearly outweigh

any risk of treatment.

Hypertonic (3%) saline solution

with or without furosemide

(which promotes free water excretion)

should be given until symptoms

subside.

It is possible to calculate the expected

change in serum sodium

concentration on the basis of the

volume of and rate at which

hypertonic saline solution is infused,

and this should be done before its

administration.

In contrast, patient with

Asymptomatic chronic hyponatremia

in

high-risk categories

(e.g., alcoholism, malnutrition, and liver

disease) is at greatest risk for

complications of the correction of

hyponatremia, namely

Central pontine myelinolysis. Such patients are best treatedwith

Water restriction

Vasopressin V2 receptor

antagonists

( Aquaretics or vaptans )

that are available in the United States for

treatment of hypervolemic and euvolemic

hyponatremia

These agents promote free water

excretion

and are useful in selected patients.

Helpful guidelines

for treatment of

hyponatremia

In patients with

Chronic asymptomatic hyponatremia

Simple free water restriction(e.g., 1000 ml/day) allows a slow and

relatively safe correction of the serum

sodium concentration.

This strategy, however, requires patient

compliance, which may be particularly

challenging in the outpatient setting.

In selected patients who are behaviorally or

physiologically resistant to free water

restriction,

Administration of salt tablets, an ADH

antagonist (e.g., demeclocycline, 600-

1200 mg/day)

or a maneuver to increase urinary solute

excretion, such as the ingestion of a

high-solute diet, may be necessary.

A difficult therapeutic dilemma is posed by

patients with neurologic symptoms and

hyponatremia of unknown duration.

Such patients are at risk for development of a

Demyelinating disorder if treated too

aggressively

yet the presence of symptoms is reflective of

central

nervous system dysfunction.

A difficult therapeutic dilemma is posed by

patients with neurologic symptoms and

hyponatremia of unknown duration.

These patients should be given treatment with

hypertonic saline solution (and furosemide if

necessary), and their serum sodium level

should be monitored every 1 to 2 hours

initially.

The rate of increase should not

exceed 8 to 10 mEq/L in a 24-hour

period.Acute therapy can be slowed once symptoms

have improved or a safe serum sodium level

(typically 120-125 mEq/L) is stably attained

(note that if the serum sodium level is extremely

low, this may require too aggressive correction

for the first 24 hours).

Central pontine myelinolysis

Central pontine myelinolysis is a rare

neurologic disorder of unclear cause

characterized by

Symmetric midline demyelination of the

central pons.

Extrapontine lesions can occur in the basal

ganglia, internal capsule, lateral geniculate

body, and cortex.

Symptoms include motor

abnormalities that can progress to

flaccid quadriplegia, respiratory

paralysis, pseudobulbar palsy,

mental status changes, and coma.

Central pontine myelinolysis is often fatal

in 3 to 5 weeks; of the patients who

survive, many have significant residual

deficits.

Alterations in the white matter are best

visualized by magnetic resonance imaging.

Central pontine myelinolysis is one of the most

feared complications of therapy for

hyponatremia.

Risk factors include a change in serum sodium

level of > 12 mEq/L in 24 hours, correction of

serum sodium level to a normal or

hypernatremic range, symptomatic and

coexistent alcoholism, malnutrition, and liver

disease.

Can hypernatremia

also occur in

Hypovolemic, Euvolemic,

and hypervolemic states?

Hypernatremia

Defined as a serum sodium

concentration greater than 145

mEq/L, occurs when too little total

body water exists relative to the

amount of total body sodium, thereby

raising the sodium concentration.

•Given that even small rises in the serum

osmolality trigger the thirst mechanism,

•Hypernatremia is relatively uncommon

unless the thirst mechanism is impaired or

access to free water is restricted.

As a result, hypovolemic hypernatremia

tends to occur in the very young, the very

old, and the debilitated.

It is typically due to extracellular fluid

losses accompanied by inability to

take in adequate amounts of free

water.

Febrile illnesses, vomiting,

diarrhea, and renal losses are

common causes.

Euvolemic hypernatremia can also be due to

extracellular loss of fluid without adequate

access to water or from impaired water

hemostasis.

Diabetes insipidus, either central (i.e.,

inadequate ADH secretion) or nephrogenic (i.e.,

renal insensitivity to ADH), results in the inability

to reabsorb filtered water, which causes

systemic hyperosmolality but

hypoosmolar (dilute) urine.

Hypervolemic hypernatremia

Although uncommon, is iatrogenic. Sodium

bicarbonate injection during cardiac arrest,

administration of hypertonic saline

solution, saline abortions, and

inappropriately prepared infant formulas

are several examples of induced

hypernatremia.

Causes of diabetes insipidus

Central diabetes insipidus

Can result from trauma, tumors, strokes,

granulomatous disease, and central

nervous system infections, and it

commonly occurs after neurosurgical

procedures.

Causes of diabetes insipidus

Nephrogenic diabetes insipidus

Can be congenital or it can occur in

acute or chronic renal failure,

hypercalcemia, hypokalemia, and sickle

cell disease, or after treatment with

certain drugs (e.g., lithium,

demeclocycline).

Signs and symptoms of

hypernatremia

In awake and alert patients, thirst is

a prominent symptom.

Anorexia, nausea, vomiting, altered

mental status, agitation, irritability,

lethargy, stupor, coma, and

neuromuscular hyperactivity are also

common symptoms.

The best therapy for hypernatremia

The first priority is circulatory stabilization

with normal saline solution in patients with

significant volume depletion.

Once normotensive, patients can be

rehydrated with oral water, intravenous 5%

dextrose in water (D5W), or even one-half

normal saline solution.

Overly rapid correction of long-standing

hypernatremia can result in cerebral

edema. Water deficit can be calculated

Some investigators have suggested that in

patients with long-standing hypernatremia,

the water deficit should be corrected by

no more than

10 mEq/L/day or 0.5 mEq/L/hr.

If the hypernatremia has occurred over a short

period (hours), it can be corrected more rapidly,

with the goal of correcting half of the water deficit

in the first 24 hours.

In addition to correcting the already established

free water deficit, daily

ongoing losses of free water in the urine and

stool and from the respiratory tract and skin

(particularly in patients with fever) should be

replaced.

In patients with central diabetes

insipidus, a synthetic analog of

ADH (i.e., 1-deamino-8-D-arginine

vasopressin) can be administered,

preferably by the intranasal route.

Helpful formulas for

assessing sodium

abnormalities

Serum osmolality

= 2 [Na+] + Glucose/l8 + Blood urea nitrogen /

2.8 + Ethyl alcohol / 4.6

Total body water (TBW)

= Body weight x 0.6 (for men)

TBW = Body weight x 0.5 (for women and the

elderly)

TBW excess in hyponatremia= TBW (1 - [Serum Na+] / 140)

Expected change in serum sodium level after

1 L 3% saline solution= (513 mEq/L – Serum [Na+]) / (TBW + 1)

TBW deficit in hypernatremia = TBW (Serum

[Na+] / 140 - 1)

Expected change in serum sodium level after

1 L D5W

= (Serum [Na+]) / (TBW + 1)

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9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY

GOOD LUCK

SAMIR EL ANSARYICU PROFESSOR

AIN SHAMSCAIRO

elansarysamir@yahoo.com