Rosen & Barkin's 5-Minute Emergency Medicine Consult (382 page)

May be asymptomatic

Review patient medication list.

• Assess volume status including skin turgor, neck veins, peripheral edema, and signs of ascites
  
• Perform a complete neurologic exam.
  

Serum sodium level:

• Recheck sodium to verify.
  

• Electrolytes, BUN/creatinine
  
• Glucose:
  
  • Correct sodium value accordingly if severe hyperglycemia (add 1.6 Na for each 100 mg/dL of glucose above normal)
    
• Calculate osmolality:
  
  • Plasma osmolality = [2 × NA (mEq L) + Glucose/18 + BUN/2.8]
    
• Urine sodium
  
• Serum and urine osmolality
  
• Thyroid function test
  
• Adrenal function tests
  
• CPK for possible rhabdomyolysis
  

• CXR to rule out CHF, infection, and tumor
  
• CT of head, particularly if patient has AMS
  

• Pseudohyponatremia due to:
  
  • Hyperglycemia
    
  • Hyperlipidemia
    
  • Hyperproteinemia
    
  • Radiocontrast dye particularly in chronic renal insufficient patients
    

TREATMENT

• Establish IV
  
• Supportive care
  

• ABCs
  
• Initiate IV fluid with 0.9% NS.
  
• Naloxone, thiamine, D
  ₅₀
  W (or Accu-Chek) for altered mental status
  

• Depends on severity and chronicity of hyponatremia and underlying etiology
  
• Chronic hyponatremia is to be corrected slowly to minimize osmotic demyelination syndrome. Correction should be limited to 10–12 mmol/L in 24 hr
  
• Acute hyponatremia with severe CNS symptoms/actively seizing:
  
  • Goal:
    
    • Raise serum sodium by 8–10mEq/L in 4–6 hr or to level >120–125 mEq/L with administration of hypertonic saline, slow or discontinue when seizure subsides.
      
    • 200–400 mL of 3% saline solution will be the approximate amount needed in most adults over the 1st 2 hr
      
    • OR may dose 1–2 mL/kg/hr of 3% saline solution
      
  • Calculate sodium deficit:
    
    • Na
      ⁺
      deficit = 0.6 (weight in kg) (140 – Na
      ⁺
      )
      
  • Sodium contents:
    
    • 1 L 0.9% NS = 154 mEq of sodium
      
    • 1 L 3% saline = 513 mEq of sodium
      
• Hypovolemic hyponatremia:
  
  • Correct underlying cause
    
  • Replete volume with 0.9% NS IV.
    
  • Primary goals to restore:
    
    • Extracellular fluid
      
    • Cardiac output
      
    • Organ perfusion
      
• Hypervolemic/euvolemic hyponatremia:
  
  • Water restriction to <1 L/day with high dietary salt intake
    
  • For faster correction of sodium:
    
    • Administer IV 0.9% NS with loop diuretic (furosemide).
      
  • Maximum rate of correction = 0.5 mEq/L/hr
    

• Furosemide: 20–40 mg IV push
  
• Sodium replacement:
  
  • Calculate Na
    ⁺
    deficit
    
  • Replace no more than 1/2 of requirement over 8–12 hr
    

500 mL–1 L of saline for a fluid challenge

• Conivaptan: Arginine vasopressin antagonist
  
• 20 mg IV loading dose over 30 min followed by 20 mg continuous IV infusion over 24 hr
  
• Tolvaptan: Selective vasopressin V2 receptor antagonist dose 15 mg/d PO and may increase in 24 hr to 30 mg
  
• Conivaptan and tolvaptan are for the treatment of euvolemic and hypervolemic hyponatremia only
  

FOLLOW-UP

• Symptomatic hyponatremia
  
• Sodium <120 mEq/L
  
• Asymptomatic, mild hyponatremia (Na
  ⁺
  120–127 mEq/L), with comorbid factors
  

• Sodium >130 mEq/L and asymptomatic
  
• Known chronic history of hyponatremia with no acute changes
  
• Asymptomatic, mild hyponatremia (Na
  ⁺
  120–129 mEq/L) with no comorbid factors; however, must have close outpatient follow-up.
  

Have repeat serum sodium within a week, particularly if related to thiazide diuretics

• Too rapid correction may cause osmotic demyelination syndrome
  
• Females, alcoholics, malnourished patients, hypokalemia, and history of liver transplant are risk factors for osmotic demyelination syndrome.
  
• Repeat and document neurologic exam during correction.
  
• Beware of falsely low sodium when blood is drawn near an IV site with hypotonic fluid.
  
• Thiazide diuretics may cause persistent hyponatremia up to 2 wk after discontinuation.
  

• Lien YH, Shapiro JI. Hyponatremia: Clinical diagnosis and management.
  Am J Med
  . 2007;120(8):653–658.
  
• Lin M, Liu SJ, Lim IT. Disorders of water imbalance.
  Emerg Med Clin North Am
  . 2005;23(3):749–770, ix.
  
• Palmer BF, Gates JR, Lader M. Causes and management of hyponatremia.
  Ann Phamacother
  . 2003;37:1694–1702.
  
• Pfennig CL, Slovis CM. Sodium disorders in the emergency department: A review of hyponatremia and hypernatremia.
  Emerg Med Pract
  . 2012;14(10):1–26.
  
• Verbalis JG, Goldsmith SR, Greenberg A, et al. Hyponatremia guidelines 2007: Expert panel recommendations.
  Am J Med
  . 2007;120(11):S1–S21.
  

See Also (Topic, Algorithm, Electronic Media Element)

Hypernatremia

CODES

• 253.6 Other disorders of neurohypophysis
  
• 276.1 Hyposmolality and/or hyponatremia
  
• 276.69 Other fluid overload
  

BASICS

• Hypoparathyroidism occurs secondary to a deficiency in parathyroid hormone (PTH)
  
• Pseudohypoparathyroidism occurs secondary to end-organ unresponsiveness to PTH
  
• PTH:
  
  • Decreases urinary Ca
    ²⁺
    loss
    
  • Increases urinary PO
    ₄
    loss
    
  • Stimulates vitamin D conversion from 25(OH)-D to 1,25(OH)
    ₂
    -D in kidney
    
  • Liberates Ca
    ²⁺
    and PO
    ₄
    from bone
    
• Hypocalcemia is the major metabolic derangement
  
• Calcitonin:
  
  • Promotes deposition of Ca
    ²⁺
    and PO
    ₄
    into bone (produced primarily in C cells in thyroid)
    
• Magnesium:
  
  • Cofactor in production of PTH
    
  • Essential for action of PTH in target tissues
    
• Hypoparathyroidism:
  
  • Primary failure of the parathyroid gland (may have associated Addison disease)
    
• Pseudohypoparathyroidism:
  
  • Tissue unresponsiveness with elevated PTH levels
    
  • Associated with hypothyroidism and hypogonadism
    
• Genetics:
  
  • Congenital absence
    
  • DiGeorge syndrome:
    
    • Hypoparathyroidism
      
    • Thymic dysplasia
      
    • Severe immunodeficiency
      
  • Wilson disease:
    
    • Destruction of gland owing to copper deposition
      
  • Autoimmune polyglandular syndrome type I
    
    • Hypoparathyroidism
      
    • Adrenal insufficiency
      
    • Mucocutaneous candidiasis
      
  • Albright syndrome (hereditary osteodystrophy):
    
    • Short stature
      
    • Obesity
      
    • Round face
      
    • Short neck
      
    • Short 4th and 5th metacarpals and metatarsals (type I pseudohypoparathyroidism)