R3 Hyponatremia and Hypernatremia

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jknell
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204171
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R3 Hyponatremia and Hypernatremia
Updated:
2013-03-09 12:35:44
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Renal II
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Renal II
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  1. Hyponatremia Definition
    -serum sodium concentration less than the normal range of 135-145 mEq/L

    **patient may have hyponatremia but have excess total body sodium and edema
  2. Hypernatremia
    -serum sodium concentration greater than the normal range of 135-145 mEq/L

    **patient may have hypernatremia but have low total body sodium
  3. Effective Osmolality
    • -"tonicity"
    • -particles which can lead to water movement across cell membranes (ignore urea)
    • -osmolality includes all particles
  4. Serum Osmolality Equation
    Posm = 2Na + glucose/18 + BUN/2.8
  5. Overview of Water Metabolism
    • -water compromises 50-70% of total weight
    • -fat contains less water than muscle (TBW dependent on body habitus)

    -most cell membranes are freely permeable to water (due to the presence of aquaporins)

    -At equilibrium ECFosm = ICFosm

    -we defend volume over tonicity (we will tolerate high or low electrolytes to maintain BP)

    • *** water only expands 1/12 into the intravascular compartment
  6. Maintenance of serum sodium concentration
    • 1. Water ingestion
    • 2. GI absorption
    • 3. Distributed throughout TBW (0.6 body weight)
    • 4. Small decrease in serum osmolality
    • 5. Suppression of ADH and Thirst
    • 6. Free water excreted by kidney

    ** serum Na+ concentration maintained within a normal range

    • -net result: temporary increase in urine flow and decrease in urine osmolality
    • -serum osmolality pretty much stays the same
    • -180 minutes after ingestion urine flow rate slows
  7. Excretion of free water
    = urinary dilution

    • -major site: thick AL
    • -minor site: cortical dilution

    *ADH MUST BE SUPPRESSED to make collecting duct water impreameable
  8. Nephron Segments Critical for Urinary Dilution
    • 1. Delivery of filtrate to medullary thick ascending limb

    2. Intact function of medullary thick ascending limb (NKCC2)

    3. ADH absent in CD
  9. Urinary Dilution: Delivery of filtrate to mTAL
    • Causes:
    • -renal failure
    • -volume depletion
    • -low "effective circulating volume"

    **enhance proximal reabsorption of NaCl and water (harder to dilute urine)
  10. Urinary Dilution: Intact function of mTAL
    • Causes:
    • -loop diuretics (inhibit NKCC2: decrease Na reabsorption/abolish medullary concentration gradient --> defects in concentrating and diluting urine)
    • -thiazide diuretics (defect in urinary dilution only)

    --> defects in urinary dilution
  11. Urinary dilution: ADH absent at Collecting Duct
    • Causes:
    • -SIADH
    • -Non-osmotic stimuli for ADH release:
    •      -volume depletion
    •      -pain
    •      -anxiety
    •      -fear

    • --> impaired dilution of urine
    • ***combinations of defects are common
  12. Why does hyponatremia develop
    -people ingest hypotonic fluids AND they cannot dilute their urine

    OR

    -water ingestion > water excretion
  13. Classification of hyponatremia
    -based on assessment of volume status

    • 1. Volume contracted or volume depleted
    • -trauma
    • -burns
    • -bleeding

    • 2. Volume overload (may have pitting edema)
    • -nephrosis
    • -cirrhosis
    • -CHF-low "effective circulating volume"

    3. Normal or "near normal" volume status
  14. Low Effective Circulating Volume and Hyponatremia
    • -all causes lead to decreased CO
    • -this results in a low effective circulating volume

    • Effects of Low ECV:
    • 1. Thirst (ingest hypotonic fluids)
    • 2. Decreased filtrate delivery to mTAL
    • 3. Increased ADH (due to hyposomolality)

    --> decreased water excretion
  15. Normal Volume and Hyponatremia
    • Excess ADH due to:
    • 1. Hypothalamic/pituitary synthesis of ADH
    • -pulmonary disease (TB, HIV, pneumonia, ARDS)
    • -drugs
    • -CNS disease (trauma, infection, tumor, MS)

    • 2. Ectopic synthesis of ADH
    • -carcinoma (SIADH due to lung carcinoma)

    • 3. Potentiation of ADH action
    • -drugs (cyclophosphamide, NSAIDS, TCAs, antidepressants)
  16. Clinical Effects
    • BRAIN SWELLING!
    • -in the setting of water overload and hyponatremia the brain swells (if there is no adaptation)

    • Acute Adaptation
    • -brain cells start exporting electrolytes to remove water

    • Chronic Adaptation
    • -other osmolytes like AAs are removed

  17. Determinants of clinical findings in hypotonic hyponatremia
    • Sx correlate with:
    • 1. severity
    • 2. rapidity

    **pts may be asymptomatic (especially with chronic hypotonic hyponatremia)

    • Symptoms (due to CNS swelling):
    • -HA
    • -N/V
    • -Confusion
    • -Seizures
    • -Coma
  18. Can drinking too much water cause hyponatremia
    -function of the amount of water ingested, the rate of ingestion and solute load

    -if minimal Uosm is 50 mOsm/L and the daily solute load is 600 mOsm then ingestion of > 12L of water could lead to hyponatremia

    --> ACUTE WATER INTOXICATION
  19. Approach to the hyponatremic patient
    • 1. Is it hypotonic hyponatremia
    • -patients may have hypertonic hyponatremia
    • -classic in patients with high blood sugar
    • -glucose pulls water out of ICF compartment, diluting Na+

    2. What is the volume status?

    3. UNa+ and Uosm

    • Low Volume:
    • 1. UNa < 10 mEq/L = Volume contraction
    • 2. UNa > 40 mEq/L = Diuretics

    • High Volume:
    • 1. UNa < 10 mEq/L = CHF, Nephrotic Syndrome, Cirrhosis (Great volume retaining states)

    • Normal Volume:
    • 1. Uosm > 300 mOsm, UNa > 40 mEq/L = SIADH, Adrenal insufficiency, hypothyroidism
    • 2. Uosm < 100 mOsm = psychogenic polydipsia (water intoxication), low solute intake
  20. Treatment of Hypotonic Hyponatremia
    • 1. Volume depleted states
    • -restore volume status with isotonic fluids
    • -water (hypotonic) will make them worse!

    • 2. Volume overloaded states
    • -water restriction
    • -ACEIs (CHF)
    • -ADH Antagonists

    • 3. Euvolemic states
    • -water restriction
    • -hypertonic saline and loop diuretics (severe hyponatremia)
    • -drugs producing a nephrogenic DI (demeclocyline)
    • -ADH antagonists
  21. Osmotic Demyelination Syndrome
    -due to rapid and/or overcorrection of hyponatremia

    -quadriparesis and pseudobulbar palsies

    -onset of sx delayed: 24-48 hours

    • To avoid rapid correction of hyponatremia:
    • -manage asymptomatic patients conservatively
    • -5-7 mEq/L increase (should reverse cerebral edema in those with sx)
    • -correction rate no greater than 0.5-1.0 mEq/h
    • -absolute correction no greater than 10-12 mEq/24hrs
  22. Morbidity and Mortality in Hyponatremia
    -mortality is higher in patients with lower Na (both total death and cardiac death)

    • Reasons for Association:
    • 1. Directly enhances mortality
    • 2. A disease process causes hyponatremia when it is more severe (mortality is a reflection of more severe disease)
    • 3. Severe disease is associated with increased mortality and hyponatremia (hyponatremia is indepently associated with enhanced mortality)
  23. Hypertonic Hypernatremia
    • -gain of solute in excess of water
    • -loss of water in excess of solute

    • Defense against hypernatremia:
    • 1. Thirst
    • -more important mechanism
    • -doesn't need a big increase in osm to increase thirst
    • -stimuli: increase osms, decreased volume, decreased BP, Ang II
    • 2. ADH
    • Clinical Correlate:
    • -pts who become hypernatremic typically cannot access water
    • -absence of ADH can be compensated for by water ingestion
    • -susceptible: very young, very old, mentally impaired, anesthetized
  24. Uosm in hypernatremia
    • 1. >800
    • -impaired thirst

    • 2. < 150
    • -complete diabetes insipidus
    • -no ADH action

    • 3. ~300
    • -osmotic agent (glucose, urea)
    • -cause water loss in urine (lots of free water loss)

    • 4. 150-800
    • -partial diabetes insipidus
    • -impaired CCM

  25. Complete Diabetes Insipidus
    • Features:
    • -low circulating ADH
    • -Uosm < 150
    • -polyuria, polydipsia
    • -responsive to ADH

    • Major Causes:
    • -neurosurgical procedures
    • -head trauma
    • -anoxic encephalopathy
    • -cancers
  26. Nephrogenic Diabetes Insipidus
    • Features:
    • -normal or high circulating ADH
    • *ADH not working at the level of the kidney
    • -Uosm < 150
    • -polyuria, polydipsia
    • -unresponsive to ADH

    • Major Causes:
    • -Li, democlocycline
    • -HIV drugs
    • -Hypercalcemia
    • -TIN, CKD
    • -Pregnancy
  27. Approach to poluria
    -urine output > 2.5 L/day

    • Uosm <150 mOsm:
    • -Complete DI
    • -psychogenic polydipsia

    • Uosm > 300 mOsm:
    • 1. 2(Na + K) < Uosm
    • =osmotic diuresis
    • -glucose
    • -urea
    • -mannitol

    • 2. 2(Na + K) = Uosm
    • =Sodium diuresis
    • -diuretic use
    • -renal salt wasting
    • -cerebral salt wasting
    • -excessive Na intake
  28. Treatment of Hypernatremia
    • 1. Assess and treat volume status
    • 2. Then address the hypernatremia
    • --> how much water will it take to correct the hypernatremia (be sure to address ongoing losses as well)

    Current TBW x Current PNa = Normal TBW x Normal PNa

    Replace no greater than 1/2 over 24 hours

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