anioin gap and dka

  1. Today in clinical, I had a patient with DKA. The doc's were wanting to monitor his anion gap and once it got down to a certain level, they were going to d/c his continuous insulin drip. The nurses I was working with couldn't remember what the anion gap had to do with insulin and blood glucose levels, and I can't figure it out either.... anyone out there have a clue?? Thanks!
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    About WSU_Ally_RN

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    PICU RN; from US
    Specialty: 7 year(s) of experience in MICU for 4 years, now PICU for 3 years!


  3. by   TheCommuter
    You can post this question on this site's Nursing Student Assistance Forums and perhaps get an answer. One of our frequent users, Daytonite, loves to give detailed answers to these types of questions.
  4. by   ICRN2008
    Here is the formula for anion gap:
    Agap = Na + K - Cl -CO2

    I would think that the doctor would be monitoring the glucose level (not the agap) to determine when to stop the insulin drip. Anyone else have an idea?
  5. by   P_RN
    One of our wonderful members Mark Hammerschmidt has a great FREE MICU site:

    Check section 4.2

    It's all acidosis/alkalosis
  6. by   thatoneguy
    ahh easy one. they are treating ketoacidosis. here is a link might better explain it than i can. but basically you ned to correct the K and P first. it pushes the glucose back into the cell thus releasing the K, also need to watch the Na.
  7. by   Daytonite
    here it is short and sweet.

    thatoneguy gave you a good link as well.

    this site also talks about anion gap. the last paragraph lists the disorders causing the metabolic acidosis. the connection with insulin and dka will be in how dka comes about (not enough insulin, so blood sugar elevates, the body homeostatic mechanisms kick in and the patient goes into dka if the situation is not treated)
  8. by   WSU_Ally_RN
    Thanks for the answers.... it makes a little more sense now!
  9. by   VickyRN
    Anion gap is defined as the difference between measured serum cations and anions. It is calculated by adding the number of chloride and bicarbonate anions together and then subtracting them from the number of sodium and potassium cations in the blood. In other words: (Na+ + K+) - (Cl- + HCO3-) where Na- is sodium, K+ is potassium, Cl- is chloride, and HCO3- is bicarbonate.

    The anion gap can be normal, high, or low. The normal level of anion gap is between 8 and 12 milliequivalents per liter of blood. An elevated anion gap reflects an increase in "unmeasured" anions--usually organic acids--that are not normally included in standard determinations of other anions, such as chloride and bicarbonate. The gap is increased when K+, Ca++, or Mg++ is decreased, when the concentration of plasma proteins is increased, or when organic anions such as lactate or foreign anions accumulate in blood. The anion gap is decreased when cations are increased or when plasma albumin is decreased.

    A high anion gap indicates metabolic acidosis. If the anion gap level is 20 or above, this signals a problem. A low anion gap is rare but may occur with multiple myeloma, hypoalbuminemia, hyponatremia, or hypomagnesemia.

    The anion gap can be used to distinguish probable cause of metabolic acidosis (high anion gap versus normal anion gap metabolic acidosis), which will aid the provider in determining a diagnosis and suitable treatment. Albumin is the major unmeasured anion and contributes almost the whole of the value of the anion gap. An actual high anion gap acidosis in a patient with hypoalbuminaemia may appear as a normal anion gap acidosis.

    Metabolic acidosis with increased anion gap may be caused by an accumulation of organic acids, such as lactic acidosis, ketoacidosis, toxic ingestions (ethylene glycol, salicylates, methanol, paraldehyde), and acute renal failure. This may also occur because of reduced inorganic acid excretion, such as that seen in chronic renal failure. Metabolic acidosis accompanied by normal anion gap may be caused by GI bicarb loss (diarrhea, ileostomy, colostomy), renal tubular acidosis, interstitial renal disease, ureterosigmoid loop, ureteroileal conduit, and ingestion of acetazolamide or ammonium chloride.

    Diabetic ketoacidosis is a serum glucose level greater than 300 mg per dL, ketones in the serum, and a pH less than 7.3 Serum sodium is often low secondary to elevated serum glucose. Serum potassium is often elevated secondary to the acidosis. Diabetic ketoacidosis is treated with insulin, fluids and correction of the electrolyte disturbances.
  10. by   ZASHAGALKA
    Some labs automatically compute the gap on their Chem7.

    Our lab doesn't. But our docs use the following formula to calculate anion gap: Na - (Cl + CO2). Technically, you add the K+ also, but there is something about offsetting lytes not on the chemistry and not including the K+ makes it more honest.

    If your sugar is high, it means your cells aren't getting that glucose because insulin is a key to the lock on the door that glucose uses to get into cells. Without glucose in the cells (it's all floating around in the blood), the cells use their alternative form of energy, lactic acid production. This, on top of the intracellular lytes that move back and forth with glucose, causes the body to become quite acidotic.

    CO2 is an acid. If you're trying to get rid of acid in your body, then you want to throw all acids overboard. CO2 can be tossed by deep rapid breathing (remember, you blow off CO2). It's actually a type of breathing characteristic to DKA - called Kussmol's Resp. It also typically has a fruity smell to it.

    The problem with acid production is that it lowers your pH. Your body works within a narrow pH range, and so this can quickly be a lethal situation. The primary initial goal of DKA treatment is to correct that acidosis. The glucose won't kill you immediately, the acid buildup will. So, glucose correction is actually a secondary goal at that point - it is important as a goal BECAUSE doing so helps to correct that acid imbalance.

    So, intially, treatment of DKA is treatment of acid inbalance. That acid production skews electrolyte lab values, causing a 'gap'. As you are 'closing the gap', it is an indication that you are treating the acidosis.

    Lots of fluids because DKA dehydrates seriously. (think 3 liters in the first 8 hrs of IV fluids). Insulin drip to get those lytes moving more freely across cell membranes in order to correct that high acid level in the blood (and to get the glucose to cells so they can stop using lactic acid production for energy). And close observation of resp status (high acid levels will probably shut down resp first -I've seen several people 'tubed' for DKA.)

    Hope this helps.

    Last edit by ZASHAGALKA on Jan 19, '06