Nephrology Book

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Hyponatremia Management

Aka: Hyponatremia Management
  1. See Also
    1. Total Body Sodium Deficit or Water Excess
    2. Hypoosmolar Hyponatremia Evaluation
    3. Hyponatremia
    4. Hyperosmolar Hyponatremia
    5. Normoosmolar Hyponatremia
    6. Sodium and Water Homeostasis
    7. Cerebral Demyelination Syndrome
  2. Approach: General
    1. See Specific Hyponatremia Management Protocols
    2. Hypoosmolar Hyponatremia (Serum Osms <280) - most cases
      1. See Hypoosmolar Hyponatremia Evaluation
      2. Hypovolemic Hypoosmolar Hyponatremia (e.g. gastrointestinal losses)
        1. Treat with Normal Saline replacement
      3. Isovolemic Hypoosmolar Hyponatremia (e.g. SIADH)
        1. Treat with water restriction
        2. Stop offending agents
          1. Stop Thiazide Diuretics permanently
          2. Stop Medication Causes of SIADH
      4. Hypervolemic Hypoosmolar Hyponatremia (edematous state)
        1. Treat with water and Sodium restriction
    3. Hyperosmolar Hyponatremia (Serum Osms >300)
      1. Typically due to Hyperglycemia
      2. Corrects with Serum Glucose normalization
    4. Normoosmolar Hyponatremia or Pseudohyponatremia (Serum Osms 280-300) - rare
      1. Serum Triglycerides >5000 mg/dl or Serum Protein >10 g/dl (e.g. Multiple Myeloma)
      2. No Sodium management required (lab abnormality only)
      3. Treat the underlying condition
  3. Management: Chronic Hyponatremia (develops over >48 hours)
    1. Chronic Hyponatremia develops gradually over days, weeks or months
      1. Cells adapt by moving solute out of cells and into the extracellular space
      2. Relatively hypotonic cells (e.g. in brain) are less likely to swell with chronic Hyponatremia correction
      3. Chronic Hyponatremia is typically asymptomatic
    2. Precautions
      1. Avoid too rapid correction of Serum Sodium
      2. Risk of Central Pontine Myelinolysis
    3. Management
      1. Known cause or volume status (hypovolemic, isovolemic, hypervolemic)
        1. Treat Hyponatremia based on Serum Osmolality, volume status and suspected cause
        2. Significant hypervolemia (edematous states) are easily identified in most cases
        3. Do not use greater than Normal Saline (e.g. avoid 3% NS) for replacement
      2. Uncertain cause, Serum Osmolality and volume status in a stable patient
        1. Start with water restriction (<800 ml/24 hours) for a few hours until likely cause discerned
        2. Chronic Hyponatremia is typically compensated and asymptomatic, allowing more time for evaluation
        3. Water restriction is effective in hypervolemic, normovolemic (e.g. SIADH) and Renal Failure cases
  4. Management: Acute Hyponatremia (<24 hours) - Less severe or asymptomatic
    1. See Total Body Sodium Deficit or Water Excess Calculation
    2. Sodium corrected faster than chronic Hyponatremia
      1. Higher risk for cerebral edema from Hyponatremia
      2. Less risk of Central Pontine Myelinolysis
    3. Known cause or volume status (hypovolemic, isovolemic, hypervolemic)
      1. Treat Hyponatremia based on Serum Osmolality, volume status and suspected cause
      2. Significant hypervolemia (edematous states) are easily identified in most cases
    4. Uncertain cause, Serum Osmolality and volume status in a stable patient
      1. Start with Normal Saline bolus with close monitoring of Serum Sodium
        1. Hyponatremia due to extracellular fluid depletion will start to correct rapidly
        2. Hyponatremia due to normal fluid status (e.g. SIADH) will minimally change
        3. Obviously avoid if possible Fluid Overload
  5. Management: Acute Hyponatremia (<24 hours) - Severe Symptomatic
    1. Indications
      1. Serum Sodium <125 meq/L with severe symptoms (e.g. lethargy, mental status changes, Seizures, coma)
      2. Emergency intervention is most critical in cases of fastest Sodium decline and most severe symptoms
        1. Rapid shifts of water into the extracellular compartment results in cerebral edema (Herniation risk)
        2. Rapidity of Sodium decline trumps the absolute Serum Sodium level
    2. Causes (most common)
      1. Hypotonic fluids (D5 1/2 NS)
      2. SIADH with excess free water intake
      3. Water Intoxication (esp. Psychosis)
      4. Significant gastrointestinal losses with excessive free water intake
      5. Cyclophosphamide IV (ADH effect)
    3. Acute stabilization of severe, symptomatic acute Hyponatremia (e.g. coma, Seizures)
      1. Give 100 ml of 3% saline over 10 minute bolus
        1. Expect an acute rise in Serum Sodium of 2-3 mEq/L with bolus
        2. Moderate symptoms may be treated with 100 ml 3% saline over 60 minutes
      2. May repeat 50-100 ml 3% bolus for as second time for persistent severe symptoms
      3. Recheck Serum Sodium every 20 minutes until symptoms improve or resolve
      4. Exercise caution due to risk of Osmotic Demyelination Syndrome
        1. Avoid a third bolus unless certain duration of Hyponatremia <24-48 hours
    4. Next correction
      1. Consider Desmopressin 1-2 mcg every 4-6 hours
      2. Sodium Infusion of 3% saline at 1-2 ml/kg/hour
        1. Increase Serum Sodium 6-8 mEq/L in first 24 hours (goal >125 mEq/L)
        2. Do not increase Sodium >10-12 mEq in first 24 hours or 18 mEq in first 48 hours
      3. Consider Diuretics in Hypervolemic Hypoosmolar Hyponatremia
        1. Furosemide (Lasix)
    5. Monitor closely in intensive care unit setting
      1. Recheck Serum Sodium every 2 hours
      2. Adjust infusion rate and change to isotonic saline as Serum Sodium improves
    6. Later correction
      1. More gradual Serum Sodium correction (e.g. 0.5 mEq/L/h or less)
      2. Treat Hyponatremia based on Serum Osmolality
      3. See Total Body Sodium Deficit or Water Excess Calculation
    7. Exercise caution, especially in patients at high risk of Central Pontine Myelinolysis
      1. Chronically ill (Alcoholism, cancer, recent Cardiac Arrest)
    8. Exercise caution in those with Congestive Heart Failure
      1. Consider concurrent Furosemide (Lasix) with caution to prevent too fast of Sodium increase
  6. Precautions
    1. Timing of the Hyponatremia and presenting symptoms dictate replacement strategy
      1. Symptomatic severe acute Hyponatremia (esp. Serum Sodium <120 mEq/L within 24 hours)
        1. Risk of severe cerebral edema and Cerebral Herniation
        2. Only indication for rapid, emergent Sodium replacement
      2. Chronic Hyponatremia
        1. Risk of Central Pontine Myelinolysis (Osmotic Demyelination Syndrome) with rapid correction
        2. Slower correction is safest option aside from symptomatic severe acute Hyponatremia
          1. In unknown Hyponatremia duration, assume chronic unless severe symptoms
    2. Follow Serum Sodium Correction closely
      1. Monitor Serum Sodium every 2-4 hours (may space to every 6 hours if consistent trend)
        1. Also monitor urine output until the Serum Sodium >125 meq/L
      2. Limit hourly correction
        1. Chronic Hyponatremia
          1. Limit correction to to <0.5 meq/L/hour
        2. Acute Hyponatremia
          1. Limit correction to <1.5-2.0 meq/L/hour
          2. If duration unclear and no serious signs or symptoms, <0.5 meq/L/hour is safest
      3. Limit daily correction to <12 meq/day
        1. Some recommend correction rate <6 meq/day
      4. Avoid overcorrection of Serum Sodium
        1. Consider agents to slow or reverse overly rapid replacement (concern for Central Pontine Myelinolysis)
          1. Initial correction
            1. Desmopressin 2-4 mcg AND
            2. D5W at 3 ml/kg over 1 hour
          2. Then resume Hyponatremia correction at slower rate
      5. Hyponatremia may worsen even with isotonic saline infusion
        1. Renal Failure
        2. Ecstasy (MDMA)
        3. Dehydration with increased ADH secretion
        4. SIADH (net fluid shift intravascularly)
    3. Avoid agents without clear efficacy
      1. Avoid Vaptans (e.g. Conivaptan, Tolvaptan) due in overcorrection risk and lack of mortality benefit
        1. Spasovski (2014) Eur J Endocrinol 170(3): G1-47 [PubMed]
  7. References
    1. Le and Drogell (2015) Crit Dec Emerg Med 29(11): 13-19
    2. Kone in Tisher (1993) Nephrology, p. 87-100
    3. Levinsky in Wilson (1991) Harrison's IM, p. 281-84
    4. Rose (1989) Acid-Base and Electrolytes, p. 601-38
    5. Braun (2015) Am Fam Physician 91(5): 299-307 [PubMed]

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