mia Treatment Guidelines 2007
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Transcript of 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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Role of vasopressin in hyponatremia
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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Role of vasopressin in hyponatremia
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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To be continue..