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I’m gonna write a book.

Actually I’m going to rewrite an old book. The Fluid, Electrolyte and Acid-Base Companion was published in 2000 but went to the printer in 1999. This book on the physiology underlying common clinical electrolyte problems was written by two residents, one in internal medicine, one in Med-Peds.

Since 1999 I have:

  • Done a year of pediatric critical care as part of Riley Children’s Hospital’s Newborn transport team

  • Completed a 2 year fellowship in Nephrology at the U of Chicago

  • Written a textbook chapter in Intensive Care in Nephrology on calcium, phosphorous and magnesium

  • Written a chapter in Principles of Critical Care, Third Edition on electrolyte issues in critical care

  • Written a review article on magnesium

  • Worked as part of the faculty for St John Hospital’s Nephrology Fellowship Program since 2003

    • So in the last nine years my knowledge and teaching sophistication on electrolytes has exploded. All this time I have been thinking about rewriting this book:

  • Fixing it

  • Adding an evidence based medicine perspective

  • Removing some of the esoteric chapters which add to the length without helping the student

  • Add resources to make it a better resource for teaching on rounds

  • Make it relevant in web based world (Think optimized for iPhone)

  • Complete revamp of Sodium with electrolyte free water

  • Finish the job we started by adding calcium, magnesium and phosphorous

    • So I’m going to write a book.
    So it begins.

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    Osmolar Gap

    The set up

    Patient without a significant medical history is admitted to the hospital comatose. The immediate differential includes alcohol ingestion

    Na 140
    K 4.0
    Cl 99
    HCO3 25
    BUN 38
    Cr 0.7
    Glucose 90
    ABG:
    7.34 / 47 / 167
    Ethanol 574 mg/dL
    Serum osmolality 442

    Step one

    What is the primary acid-base disorder:
    The pCO2 is up and so is the bicarb, so this is respiratory acidosis.

    Step two

    Is the compensation appropriate:
    for every 10 the pCO2 is increased the bicarb should rise 1 if the disease is acute and 3 if it is chronic. In this case we presume the respiratory disorder is due to the intoxication so it is acute, so the bicarb should rise 0.7 or close to one because the pCO2 is 7 above 40 (normal). The actual bicarbonate is 25 so this is an appropriately compensated acute respiratory acidosis.
    If this patient had chronic respiratory acidosis, then the bicarbonate should rise to 26 (0.7 x 3 =2.1).

    Step three

    Is there an anion gap?
    140 – (99+25) = 16. Yes. But it is very small.

    Step four

    Is there an osmolar gap?
    Calculated osmolality = 2 x Na + Glucose / 18 + BUN / 2.8 + Ethanol / 3.7
    2×140 + 90/18 + 15/2.8 + 574/3.7 = 280+5+5.4+155 = 445.5
    Osmolar Gap = Measured Osm – Calculated osmolality
    Osmolar Gap = 442 – 445 = -3

    Step five

    No significant anion gap and no osmolar gap means that this is just ethanol toxicity.
    Many medical calculators use 4.6 as the divisor for the osmolar gap. However empiric data shows that ethanol does not act as ideal solute and the divisor should be 3.7. If you use 4.6 the osmolar gap comes out to be: 442 – 415 = 26.

    Step six

    This is simple alcohol intoxication. No indication for fomepizole or dialysis. Ethanol is highly dialyzable. The indications for dialysis is hemodynamic instability despite pressers and volume resuscitation. This patient has depressed mental status and depressed respiration. The treatment for this is supportive care, not dialysis.