Nicole Kupchik

Author, Independent Clinical Nurse Specialist & Educator

Critical Care Consulting | Quality Improvement/Program Development | Critical Care Education | Certification Reviews

When I left the Cardiac-Surgical ICU to go to a Medical Cardiac ICU at a Level I Trauma center, it was a big change for me. It was a whole new regime of policies, protocols, and procedures.  And, it was a big chance for growth for me as a nurse.

I remember one of the first patients I had when I got to the new unit.  I was caring for a DKA patient and the doctors continually asking me “has her gap closed?”  I thought to myself, “What the heck are they talking about?”


Diabetic Ketoacidosis:  What is it?

Diabetic ketoacidosis is an EMERGENCY!  It must be treated as quickly as possible to prevent coma and/or death. The patient’s insulin needs are unable to match their insulin supply.  The body metabolizes glucose for energy, so it begins to metabolize fats and acids, which in turn, create ketones.  The ketones create keto acids, which create a state of acidosis.


Watch this video for an in-depth conversation about DKA:


What are the signs of DKA?

  • Nausea and vomiting
  • Kussmaul’s breathing
    • Irregular pattern of deep & rapid breathing. Patient’s are trying to blow off CO2 to lower acid levels
  • Tachycardia
    • Related to extracellular hypovolemia
  • Fruity Breath
    • Caused by the metabolizing of ketone bodies
  • Dry mouth
  • Frequent urination
    • Osmotic diuresis
  • Lethargy, tired, drowsy, confusion
    • Related to hyperosmolar state


Who is at risk for DKA?

  • Type I Diabetics
    • DKA can often be the first manifestation of Type 1 diabetes.

Chronic hyperglycemia causes damage to tissues & organs over time.  The body can (for the most part) tolerate and compensate while the person is young.  Additionally, younger people and children burn more calories (thus, lowering their glucose levels) than adults due to:

  • Growth & growth hormones
  • Active lifestyles

What converts the person from a state of tolerance to a state of DKA, is an injury.  Injuries are not just a physical injury like a cut or something, but any type of injury which causes the body to develop a stress response to repair itself, like infection.


Overdrive factors (Brutsaert, 2017):

  • Infection (i.e. bacterial, viral, or fungal)
    • Pneumonia
    • UTI
  • Medications
    • Lack of Insulin (if known diabetic)
    • Interaction of other medications
    • Steroids
    • Diuretics
  • Big events (less likely for younger patients)
    • Stroke
    • Myocardial Infarcts
    • Trauma
  • Alcohol use/abuse


What is an Anion Gap?

An Anion Gap is the difference between the measured cations and anions in the serum.

There are some formulas where potassium is not added to the sodium.  The rational behind that is potassium is usually a small number and may not affect gap all that much.  **However, in DKA, it can be the difference between reaching your goal directed therapy markers or your patient still being in a state of acidosis and dehydration.


The Role of the Anion Gap in DKA:

When my doctors were asking about the patient’s gap being “closed”, they were talking about the balance of cations and anions.  The tricky part about DKA is that the gap isn’t necessarily related to just sodium, potassium, chloride, or bicarbonate.  The metabolism of fats and acids produce ketoacids, which are not directly measured.

A low sodium level may also affect the anion gap.  Sodium levels will also be falsely low due to the increase in glucose. This is due to the shift of free water from intracellular to extracellular fluid.  As the glucose is corrected, then free water shifts back and serum sodium corrects to actual values.

Na+ is 7-10 mEq/L lower for every 100 mg/dL

            I.e. Blood Glucose is 500 mg/dL = Na+  28 – 40 mEq/L lower than actual

As the glucose levels fall with fluid and insulin therapy, the process of ketosis begins to decline.  The body then begins to metabolize glucose again.  Closing the gap demonstrates that serum levels of electrolytes and acid base balance are normalized.

Once the Gap is less than 11 mEQ/L, it is considered closed.  At this point, we begin to transition patients from an emergent stage of treatment to an intermediate or final phase.  Intermediate or final phases of treatment include:

  • Resuming their diet
  • Gentle fluid replacement (hypotonic – see below)
  • Subcutaneous insulin treatment
    • Long acting
    • Short acting


How do you treat DKA and the Anion Gap?

  1. Volume:
    1. Calculate free water deficit to determine fluid goals:
      1. 6 (kg) x [(Current Na+ /Goal Na+ 140)-1]
      2. e 0.6 x 100 x [(154/140)-1] = 6 liters
      3. Serum Osmolality can demonstrate adequate resuscitation as the levels drop less than 300 mmol/kg
    2. Initial resuscitation with an isotonic solution (may require 3 – 5 liters or more)
    3. Transition to a 0.45% Saline + Dextrose Solution with potassium (A hypotonic solution? Wait, what… Why? Well, once the extracellular volume is replaced the cells are still dehydrated from the earlier shifting.  Now, we have to hydrate the cells)
  2. Insulin:
    1. Do not treat glucose until Potassium is greater than 3.5 mEq/L
      1. **Insulin will shift potassium into the cell causing further hypokalemia
    2. Usually with an insulin infusion for 24 hours for tight control
    3. Transition to long acting and short acting as gap closes and the glucose normalizes
  3. Phosphate:
    1. Hypophosphatemia
    2. Often we do not treat!! Treatment may result in hypocalcemia
    3. If you do decide to treat, potassium phosphate will also help correct the potassium levels
  4. Sodium Bicarbonate:
    1. National shortage!!
    2. Only if pH on ABG is less than 6.9
    3. Fluids and insulin will correct this naturally, there is a high threshold for administration
  5. Treatment of initial injury mechanism:
    1. Infection (antibiotics, antiviral, or antifungals)
    2. Resolution of major events (i.e. MI, stroke, trauma)
    3. Resume an insulin regimen
    4. Stop medications which may interact with insulin or cause resistance
  6. Monitoring:
    1. Neurological status = Cerebral edema & hyperosmolality
    2. Respiratory status = Metabolic acidosis with uncompensated respiratory alkalosis
    3. Serum studies: Anion gap, osmolality, potassium, and glucose
    4. Urine output



The treatment of DKA requires close monitoring of many laboratory values.  Clinicians need to be able to know the normals, as well as, the calculated variables related to shifting of fluids and electrolytes.  The use of anion gap is a helpful tool for medical and nursing providers to understand the state of ketosis and metabolism balance in the treatment of DKA.

DKA is a medical emergency.  DKA is something that any nurse can see in any department.  With patients who visit us in the clinic or hospital, we need to be aware of the signs and symptoms of DKA so that we can get patients treatment as quickly as possible.




Brutsaert, E. F. (2017). DKA. Retrieved January 20, 2018 from

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