Hyponatremia

Pathophysiology

• Excess of water relative to sodium: almost always due to t ADH

• t ADH may be appropriate (eg. hypovolemia or hypervolemia with I EAV)

• T ADH may be inappropriate (SIADH)

• Rarely, i ADH (appropriately suppressed), but kidneys unable to maintain nl [Na]„nm primary polydipsia: ingestion of massive quantities (usually -12 L d) of free H2O overwhelms diluting ability of kidney (normal solute load 750 mOsm d, min U«™ 60 mOsm L . excrete in 12 L if H2O ingestion exceeds this. HjO retention) "tea & toast" and "beer potomonia": 11 daily solute load. T free HjO insufficient solute to excrete H2O intake (eg. if only 250 mOsm d. minimum Uw 60 mOsm L -» excrete in -4 L: if H2O ingestion exceeds this. H20 retention) Workup inejm 2000.342:1581)

• Measure plasma osmolality

Hypotonic hyponatremia most common scenario: true excess of free HjO relative to Na Hypertonic hyponatremia: excess of another effective osmole (eg.glc. mannitol) that draws HjO intravascular!^ each 100 mg di Í glc >100 mg dl — i [Na] by 14 mEq l Isotonic hyponatremia: rare lab artifact from hyperlipidemia or hyperproteinemia

• For hypotonic hyponatremia. / volume status (vital signs, orthostatics. JVP. skin turgor, mucous membranes, peripheral edema. BUN. Cr. uric acid)

• Uoun diagnostically useful in limited circumstances, because almost always -300

exceptions: Uown 100 in 1° polydipsia & I solute intake moreover. U^m 300 * SIADH: must determine if T ADH appropriate or inappropriate however. U^, important when deciding on treatment (see below)

• If euvolemic and t U««. evaluate for glucocorticoid insufficiency and hypothyroidism

Figure 4-4 Approach to b; porta t/emu

Hypotonic Hyponatremia

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euvolemic hypervolemic

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Euvolemic

Hypervolemic

Hyponatremia

Hyponatremia

Hyponatremia

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U^ylOO U^r, <100 Ua

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CHF Renal

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Cirrhosis failure

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Nephrosis

Hypovolemic hypotonic hyponatremia

• Renal losses (Un, >20 mEq L FEn. >1%): diuretics (espec. thiazides, as loop diuretics

I tonicity of medullary interstitium and impair urine concentrating ability), salt-wasting nephropathy, cerebral salt wasting, mineralocorticoid deficiency

• Extrarenal losses (Un, 10 mEq L FEn, < 1%): Gl losses (eg. diarrhea), third-spacing

(eg. pancreatitis), inadequate intake, insensible losses

Euvolemic hypotonic hyponatremia

• SIADH (eu- or mild hypervolemia, inappropriately * Uov». normal Un*. 4 BUN & uric acid)

pulmonary: pneumonia, asthma. COPD. SCLC. PTX. ® pressure ventilation intracranial: trauma, stroke, hemorrhage, tumors, infxn. hydrocephalus drugs: antipsychotics, antidepressants, chemotherapy, vasopressin. dDAVP miscellaneous: pain, nausea, postoperative state

• Endocrinopathies: t ADH activity seen in glucocorticoid deficiency (co-secretion of

ADH & CRH) and hypothyroidism (1 CO & i GFR)

• Psychogenic polydipsia (Uowi <100.1 uric acid): usually requires intake 12 L d

• Low solute: "tea & toast": "beer potomania"

• Reset osmostat: chronic malnutrition (i intracellular osmoles) or pregnancy (hormonal effects) -* ADH physiology reset to regulate a lower [Najwrum

Hypervolemic hypotonic hyponatremia

• Cirrhosis (splanchnic arterial vasodilation and ascites --»i EAV;Un, < 10 mEq LFEn, • 1%)

• Nephrotic syndrome (hypoalbuminemia — edema i EAV;Un, <10 mEq LFEn, 1%)

Treatment

• Goals of treatment

Asymptomatic hyponatremia: correct [Na]**,™ at rate of ^.0.5 mEq L h Symptomatic hyponatremia: initial rapid correction of Na (2 mEq L h for the first

2-3 h) until sx resolve Rate of T Na should not exceed 10-12 mEq L d to avoid osmotic demyelination syndrome (spastic quadriplegia, dysarthria, dysphagia), espec if hypoNa chronic

• Effect of IV fluids initial per L .nfusate - ' t^l— ™w „60 , IBW„ eu»*

eg. 1 L hypertonic saline (513 mEq Na) given to 70 kg (IBW) man w [Na] 110 mEq L will T [Na]».™, by 9.4 mEq however, above assumes entire infusatc retained without any output of Na or H2O if Pt is euvolemic. as in SIADH. then infused Na will be excreted eg. 1L NS (154 mEq of Na or 308 mOsm of solute in 1L free HjO) given to Pt with SIADH with Uov* 616 - 308 mOsm solute excreted in 0.5 L HjO -net gain 0.5 L H20 - i [Na]

.-. normal saline can worsen hyponatremia 2° SIADH if U0tm > infusateovr,

• Hypovolemic hyponatremia: volume repletion with normal saline once volume replete stimulus for ADH removed — kidneys will excrete free HjO — serum Na will correct rapidly

• SIADH (N£/M 2007:3562064): free water restrict * treat underlying cause hypertonic saline (t loop diuretic) if sx or Na fails to T w free HjO restriction 1 L hypertonic saline will raise [Na]^ by 10 mEq (see above)

50 ml h will t [Na] by 0.5 mEq L h; 100-200 ml h will T [Na] by 1-2 mEq L h formula only provides estimate:.. recheck serum Na frequently demedocydine or Li: cause nephrogenic Dl aquaresis with conivaptan (Via andV2 vasopressin receptor antagonist)

• Hypervolemic hyponatremia free water restrict

T EAV (eg. vasodilators and loop diuretics to T CO in CHF. colloid infusion in cirrhosis) ? aquaresis with tolvaptan (V2 vasopressin antagonist) (SALT-1 & SALT-2. ne}m 2006:355:2099)

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