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Water Balance

This document discusses the various mechanisms of hyponatremia and hypernatremia. It describes six categories: hypotonic, isotonic, hypertonic, hypovolemic, euvolemic, and hypervolemic hyponatremia as well as central and nephrogenic diabetes insipidus which cause hypernatremia. For each category it provides details on expected lab values, urine osmolality and volume, and underlying pathophysiological causes. Treatment options are also mentioned.

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Brian Wong
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44 views3 pages

Water Balance

This document discusses the various mechanisms of hyponatremia and hypernatremia. It describes six categories: hypotonic, isotonic, hypertonic, hypovolemic, euvolemic, and hypervolemic hyponatremia as well as central and nephrogenic diabetes insipidus which cause hypernatremia. For each category it provides details on expected lab values, urine osmolality and volume, and underlying pathophysiological causes. Treatment options are also mentioned.

Uploaded by

Brian Wong
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Mechanism

Plasma Osmolality 275-295 (Nl)

Plasma [Na+] <136 <136 mEq/L

Urine [Na+] mEq/L < 10

Urine Osm mOsm/Kg H2 O >400

BUN/Creatinine

Isotonic Hyponatremia

Lab Artifact due to increased lipids and proteins

15:1

Hypertonic Hyponatremia

[Glucose] in plasma draws water out from cells; giving a falsely low [Na+]

>295

2 mEq/L for each glucose by 100 above 100

< 10

>400

15:1

Hypotonic Hyponatremia - Plasma tonicity decreases with plasma [Na+]


-Hypovolemic intravasc. Vol. (orthostatic hypoTN, tachycardia, low JVP) (1) more Na+ is lost than H2 O or (2) losses in Na+ and H2O are replaced by pure H2O Renal losses: impaired Na+ reabsorption in distal tubules and cortical collecting ducts Aldo deficiency Thiazide-type diuretics Tx: Isotonic Saline

<275

<136 mEq/L

> 20 >400 (Though RAAS is (intravasc. stimulated, vol stimulates Na+ reabsorption ADH) is impaired) >100 (Not as high, since Na+ losses and polyuria prevent formation of a hypertonic medullary interstitium; however ADH is still active)

20:1 (decreased intravasc. volume)

polyuria

Cerebral Salt Wasting (CSW) BNP-mediated increase in GFR

<275

<136 mEq/L

>20 (BNP-mediated GFR => RAAS => Na+ reabsorption)

20:1 (decreased intravasc. volume)

Non-renal losses: vomiting, secretory diarrhea, or excessive sweat -Hypervolemic intravasc. Vol. (Edema, JVP) Pt. retain more H2O than Na+

<275

<136 mEq/L

<10 (RAAS is active, and unopposed)

>400 (ADH is active)

20:1 (decreased intravasc. volume)

DRUG OF CHOICE: Tolvaptan (for non-renal only) Tx: Na+ and H2O restriction ~300 (failing kidneys unable to dilute or concentrate urine, isotonic to plasma) >400 (intravasc. vol turned on ADH)

intravasc. Vol. Renal retention: ATN and (effective) chronic kidney failure

<275

<136 mEq/L

>20 (cant reabsorb Na+)

15:1 (Na+/H2O/BUN) reabsorption is impaired

Non-renal retention: CHF, intravasc. Vol. Cirrhosis, and nephritic (effective) syndrome -Isovolemic intravasc. Vol. (no edema, JVP Nl; look Nl on exam)
DDx w/ SIADH: (1) Glucocorticoid deficiency: ACTH disinhibits ADH release (2) Hypothyroidism: CO => GFR => nonosmotic release of ADH (3) Carbamazepine: ADH release (4) NSAIDs, chlorpropamide: ADH action (5) Exercise: IL-6mediated inflammation polyuria (3 L/day)

<275

<136 mEq/L

<10 (RAAS is activated by intravasc. vol (effective)

20:1 (effective intravasc. vol)

Retention of electrolyte free H2O

DRUG OF CHOICE: Conivaptan (V1a/V2 receptor antagonist); blocks ADH!! TX: Water restriction

SIADH H2O retention and Na+ excretion Inappropriate inflammation-mediated release of ADH (IL-6) <275 <136 mEq/L

>20 (RAAS is inhibited by retention of H2O => GFR)

>100 (may or may not be higher than plasma)

15:1 (<10) (w/out RAAS)

(6) Primary psychogenic polydypsia

<275

<136 mEq/L

>20 (RAAS is inhibited by drinking 20L of

<100 (drinking so much water, that dilutes

15:1

pure H2O) -Hypovolemic loss of more H2O than Na+ renal medulla has Renal losses: interstitial tonicity => -loop diuretics => intravasc. less driving force to suck up water from vol. depletion
lumen
orthostatic hypoTN tackycardia

the urine)

Hypernatremia: inadequate H2O intake => hypertonicity of the ECF compartment


>295 >145 mEq/L Tx: Hypotonic Saline >20 <600 (large amts. of (intravascular Na+ being volume secreted in urine) depletion) >300-350 >20 (kidneys are (large amts. of unable to + Na being reabsorb Na+ secreted in urine) and urea) <10 >600 (RAAS is (ADH is stimulated by stimulated by IVD) IVD) Tx: Water replacement <100 (ADH doesnt work at all) 20:1 (intravascular volume depletion) 15:1 (No IVD) 20:1 (IVD) 15:1 (w/o absorbing Na+/H2O, BUN wont go)

-osmotic diuresis -chronic kidney dz

>295

>145 mEq/L

UO < 500 mls/day

Non-renal losses: -excessive sweat -osmotic diarrhea electrolyte-free H2O loss Total body Na+ is normal Central DI: ADH secretion -head trauma, -craniopharyngioma

>295

>145 mEq/L

20:1

-Isovolemic

Nephrogenic DI: ADH activity in kidney - lithium -demeclocycline more Na+ than H2O -Hypervolemic addition administration of NaCl and NaHCO3 solutions:

polyuria (18-20L/day)

>295

>145 mEq/L

edema, JVP

>295

>145 mEq/L

>100 (ADH partially works) DOC: Thiazide Diuretics Tx: Water replacement >600 (since >40 hypertonicity (RAAS is being inhibited) => ADH secretion)

<10 (RAAS is okay)

15:1 (no intravasc. vol depletion)

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