mia Treatment Guidelines 2007

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Hyponatremia

treatment guidelines2007

The American journal of Medicine (2007) vol 120

(11A), S1-S21


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Introduction Hyponatremia is the most common disorder of

electrolytes in clinical practice

15% to 30% of both acutely and chronicallyhospitalized patients

Hyponatremia is important clinically because:

(1) Acute severe hyponatremia substantialmorbidity and mortality

(2) Rapid correction severe neurologic deficitsand death.


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Role of vasopressin in hyponatremia

AVP secretion is normally stimulated by:

Increased plasma osmolality via activation

of osmoreceptors located in the anteriorhypothalamus

Decreased blood volume or pressure via

activation of baroreceptors located in thecarotid sinus, aortic arch, cardiac atria,and pulmonary venous system


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When osmolality falls plasma AVP levelsbecome undetectable and renal excretionof solute-free water (aquaresis) results to

prevent decreases in plasma osmolality Failure to suppress AVP secretion at

osmolalities below the osmotic thresholdresults in water retention and

hyponatremia.


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In SIADH, despite hypo-osmolality AVP release is notfully suppressed owing to a variety of causes, includingectopic production of AVP by some tumors.

The persistence of AVP release due to nonosmotichemodynamic stimuli is also predominantly responsiblefor water retention and hyponatremia with hypovolemia,as well as in edema-forming disorders such as heartfailure and cirrhosis

Vasopressin receptor antagonist


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Classification and differential diagnosis of hyponatremia

Hypo-osmolality indicates excess water

relative to solute in the extracellular fluid

(ECF) compartment.

Because water moves freely between the

ECF and the ICF compartments, an

excess of total body water relative to totalbody solute is present as well.


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Hypotonic Hyponatremia The osmolality of body fluid within narrow limitsregulated by AVP secretion and thirst

Between 280 and 295 mOsm/kg H2O. Only solutes that are impermeable to the cell

membrane and remain relativelycompartmentalized within the ECF are effectivesolutes

Sodium and its accompanying anions are themajor effective plasma solutes

Hyponatremia=hypo-osmolarity except..


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Pseudohyponatremia Marked elevation of lipids or protein in

plasma can cause artifactual decreases in

serum sodium because of the larger

relative proportion of plasma volume that

is occupied by the excess lipids or proteins

Isotonic hypernatremia


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Isotonic or hypertonic hypernatremia

Effective solutes other than sodium are

present in the plasma

Hyperglycemia, mannitol, contrast media


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Pathogenesis of hypotonic hyponatremia

Water moves freely between ICF and ECF

Solutes = Na, K

Hypo-osmolarity = excess of body water,depletion of body solute


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Classifications and diagnosis of

hypotonic hyponatremia

ECF volume status and urine sodium

excretion

Hypovolemic

Euvolemic

Hypervolemic


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Hypovolemic hyponatremia

Body solute depletion

Intravascular volume cannot be easily measured directly

History, PE and lab results Orthostatic hypotension, dry mucus membranes,

decreased skin turgor

Elevated BUN, creatinine, BUNcreatinine ratio, and uricacid level (affected by dietary protein intake, steroid)

spot urine [Na+] should be


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Euvolemic hyponatremia SIADH

History, PE and lab results

Without clinical signs of volume depletionor volume expansion(subcutaneousedema, ascites)

Normal or low BUN, low serum UA Spot urine Na > 30 mmol/L


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Hypervolemic hyponatremia

Increased ECF volume body Na excess

Effective arterial blood volume (EABV) waterexcretion body water

Increases the reabsorption of glomerular filtratenot only in the proximal nephron but also in thecollecting tubules by stimulating AVP secretion.

Clinical signs of volume overload

BNP(brain natriuretic peptide)

Spot urine Na < 30 mmol/L due to activation ofRAAS with secondary renal sodium conservationdespite the whole body volume overload.


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Etiologies and Pathophysiologies of

hypotonic hyponatremia

GI disease

Excessive sweating

Diuretic therapy

Cerebral salt wasting

Mineralocorticoid deficiency


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GI disease

Gastric contents and stool are hypotonic

Protracted vomiting or diarrhea without replacement offluid volume depletion and hypernatremia.

However, if patients ingest fluid and food low in sodium

content baroreceptorAVP secretion hyponatremia Volume depletion

Urine Na will be low, but may be elevated with ongoingvomiting, because bicarbonaturia obligates excretion ofan accompanying cation.

Urine Cl should be low


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Excessive sweatingAfter vigorous exercise such as marathon

Loss of sadium and chloride in sweat

during exercise

More recent evidence indicates that

excessive water retention is principally

responsible


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Diuretic therapy High urine Na

73% thiazides alone (days to weeks)

typically are elderly women

20% thiazides + antikaliuretics

8% furosemide (months)


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Cerebral salt wasting

Occur after head injury or neurosurgical

procedures

Loss of sodium and chloride in the urine

intravascular volume baroreceptor

AVP secretion water retention

hyponatremia Superficially, CSW resembles SIADH


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Mineralocorticoid deficiency Primary adrenal insufficiency caused by

adrenal destruction or hereditary enzyme

deficienciesrenal sodium wastinghypovolemia and a secondary volumestimulus to AVP release water retention hyponatremia

High urine Na and hyperkalemia

Low urine K or TTKG


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Euvolemic hypernatremia SIADH

Nephrogenic syndromes of inappropiate

antidiuresis Glucocorticoid deficiency

Hypothyroidism

Exercise associated hyponatremia (EAH)

Low solute intake

Primary polydipsia


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Nephrogenic syndrome of inappropriate

antidiuresis

Genetic mutations of the V2R activation

of antidiuresis in the absence of AVP-V2R

ligand binding

Met diagnosis of SIADH except low

plasma AVP level


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Glucocorticoid deficiency

Isolated glucocorticoid deficiency occurs with

secondary adrenal insufficiency, generally

caused by pituitary disorders that impair normalACTH secretion but leave other stimuli to

aldosterone secretion intact.

That glucocorticoid deficiency alone also impairs

water excretion was recognized based onlongstanding clinical observations


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Hypothyroidism

Hyponatremia secondary to hypothyroidism occurs muchless frequently than hyponatremia from adrenalinsufficiency.

Severe hypothyroidism elderly myxedema coma

Primary hypothyroidism When hyponatremia accompanies hypopituitarism it is

usually a manifestation of secondary adrenalinsufficiency from glucocorticoid deficiency rather thancoexisting hypothyroidism.

Thyroid hormone cardiac output EABVAVPsecretion


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Low solute intake

Ingest large volumes of beer with little foodintake for prolonged periods (beer potomania)

Because 50 mOsmol of urinary solute excretion

are required to excrete each liter of maximallydilute urine.

Consequently, water retention withhyponatremia will result when fluid intake

exceeds the maximum volume of urine that canbe excreted based on the available solute

No role of AVP


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Primary polydipsia

Psychiatric patients schizophrenia

141mmol/L at 7 AM to 130mmol/L at 4 PM

Although no single mechanism can completely

explain the occurrence of hyponatremia in

psychiatric patients with polydipsia

The combination of higher than normal water

intake plus even modest elevations of plasmaAVP levels from a variety of potential sources


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Hypervolemic hyponatremia

Heart failure

Liver cirrhosis

Nephrotic syndrome, acute and chronic

renal failure


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Heart failure

20% of patient

Atrial-renal reflex

Henry-Gauer reflex Increase in left atrialpressure suppreses the release of AVP waterdiuresis

An increase in transmural atrial pressure is alsoknown to increase atrial natriuretic peptide (ANP)secretion increase in sodium and water

excretion. A decrease in renal adrenergic tone is another

reflex that normally occurs with an increase inleft atrial pressure


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Cirrhosis

30-35% of patients

Nonosmotic release of AVP

Baroreceptor mediated or other neurohormonal

factors have not been clearly established

This conclusion is derived from studies in

cirrhotic patients receiving an AVP V2R

antagonist that demonstrate urinary dilution andincreased serum [Na+].


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Nephrotic syndrome, acute and chronic

renal failure

Hyponatremia occurs commonly in both acuteand chronic renal failure, because the kidneyscannot maximally excrete excess ingested or

infused water. In contrast, hyponatremia is not very common in

the nephrotic syndrome unless associated with asubstantial decrease in GFR

Severe hypoalbuminemia < 2 g/dL

intravascular hypovolemia Non-osmoticrelease of AVP water retention


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mia Treatment Guidelines 2007

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