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Sodium balance (Hypernatremia (= hypertonicity) (Treatment (address ECF…

- - - - renal causes
        
        examples
        
        water diuresis (e.g. diabetes insipidus)
        
        loss of mainly water without solute, usually due to either central DI or nephrogenic DI (defect of ADH secretion or ADH action)
        
        central DI - absence of ADH from pituitary
        
        tumors, infiltrative disorders, trauma, infections
        
        nephrogenic DI - ADH resistance
        
        congenital forms
        
        drugs (lithium, foscarnet - antiviral drugs used for CMV in AIDS patients, and herpes lesions)
        
        electrolyte disorders (hypokalemia, hypercalcemia)
        
        interstitial diseases of the kidney
        
        osmotic load < 900 mosm/day
        
        urine osmolality < plasma osmolality, usually < 150 mosm/L
        
        osmotic diuresis (glucosuria in diabetes, etc.)
        
        loss of water due to solute osmotically preventing water reabsorption in the tubules - most often seen with glucosuria, tube feeds, etc.
        
        osmotic load > 900 mosm/day
        
        urine osmolality > plasma osmolality (ie ADH is acting). between DCT and CD the osmolality outside the tubule is about 300 mosm/L.
      - non-renal causes
        
        examples: burns, profuse sweating, hypotonic GI losses
        
        in the face of non-renal water loss, the kidney should be able to minimize urinary volume via concentration -- in most cases it can concentrate up to 1200 mosm/L (a minimum of 600 mosm/L)
    - - characterized by hypervolemia on exam and increase in weight
      - examples: hypertonic saline given rapidly in the ICU, sodium bicarbonate ampules, etc.
- - - - Inadequate GFR
        
        GFR < 20 cc/min
        
        Examples: advanced renal disease or sudden acute renal failure
      - Compromised diluting segments
        
        TAH
        
        Example: loop diuretics do not cause significant hyponatremia (due to the countercurrent multiplier, these agents disrupt the ability to dilute in the TAH but also the ability to concentrate in the CD - effects on sodium cancel out more or less)
        
        DCT
        
        Example: thiazide use (can cause severe hyponatremia)
      - Inadequate osmotic load
        
        lower ingestion of osmoles = less urine that can be produced
        
        Example: beer potomania (a case of low solute intake)
      - ADH presence
        
        segment most commonly involved in hyponatremia
        
        clinically noted by increased urine osmolality
        
        physiologic stimuli for ADH release
        
        increased tonicity (sensitive to a 1% change in osmolality) -- conversely, a urine osmolality < 100 mosm/L is an appropriate response to a water load because ADH action decreases (anything > 100 mosm/L is an inappropriate response to a water load)
        
        decreased effective circulating volume status (~10% reduction required) is the most potent stimulus of ADH release
        
        other causes: nausea, various drugs (NSAIDs, SSRI, etc.), pain, decreased cortisol level (adrenal insufficiency), decreased T4 level (myxedema coma) all affect ADH release independent of osmolality
        
        non-physiologic stimuli for ADH release (SIADH)
        
        brain tumor
        
        pulmonary processes
        
        lung lesion: tumors of the lung (ectopic secretion of ADH; small cell malignancy), ventilators (expansion of alveoli), tuberculosis, pneumonia
        
        idiopathic
        
        brain lesion
    - - symptoms: confusion, seizures, etc. (risk of herniation). If someone is symptomatic give 3% saline (hypertonic solution). asymptomatic: conservative treatment
      - aggressive treatment: rapid sodium administration will raise the serum sodium. Although sodium is restricted to the ECF, it affects osmolality in the ICF as well because water moves freely between both compartments. Any sodium calculation must assume that you are adding sodium to the entire TBW. Example: correct by 5 meq in the first 4-6 hours or until patient stops seizing
      - conservative treatment: goal is to get rid of excess water. Quantify how much water is being excreted and ensure free water intake < free water excretion. Loop diuretics, vaptan agents (decrease ADH), higher osmolar loads (urea/salt tablets), restrict free water intake
      - Chronic hyponatremia correction: > 3 days duration is associated with adaptations that try to minimize the degree of cellular swelling. As there is hypoosmolality in the ECF, the ICF attempts to correct for this by extruding osmoles from the brain. Don't correct too quickly! don't wait it to shrink suddenly --> results in osmotic demyelination syndrome ODS. Results in paralysis