Written by Van Wall, DO
Edited by Nicholas Thompson, MD

CASE: 12 yo girl presents with her mom for respiratory distress.  Mom states that over the past month her daughter has lost approximately 25lbs, has had increased thirst, fatigue, and is going to the bathroom constantly.  Last night she began breathing faster and more heavily and was speaking in short sentences.  Her skin has had a lacy appearance today.  She denies any recent illnesses, fevers, cough, nausea/vomiting, or diarrhea.  She had her last menstrual period approximately 2 weeks ago which was normal.

VS: 155, 110/82, 98%ra, 30, 98.6
HPI, POCT glucose 500+ , Kussmaul respirations and mottled skin highly indicative of DKA.  Extreme metabolic and electrolyte derangements are hallmarks of this diagnosis.  This is often the first presentation, but more frequently due to  medication non-compliance in a known diabetic or from a recent stressor or infection.
Other presenting symptoms may include:
  • nausea/vomiting, abdominal pain (muscle cramps may present as an acute abdomen)
  • recurring candidal infections
  • new onset enuresis
  • fruity/ketotic breath (due to acetone production)

Diagnosis officially based on:

  •  Hyperglycemia with blood glucose concentration greater than 200 mg/dL
  •  Venous pH less than 7.3 or bicarbonate concentration less than 15 mmol/L
  •  Ketonuria and ketonemia
As always, a quick assessment of airway, breathing, circulation and mental status are critical.  These patients may be severely acidotic, and are usually extremely dehydrated.  If they are protecting their airway, then intubate only as a last resort.  The Kussmaul respirations are compensatory and stopping this may worsen the acidosis.  Make sure they are hooked up to the monitor with continuous telemetry and O2 sats.
  • You want to know immediately: glucose, anion gap, electrolytes, bicarb, pH, osms and also consider any precipitating cause such as infection, pregnancy/ectopic, AMI.  Get an ECG and send urine studies, cultures, do a chest x-ray and assess for any skin lesions or cellulitis.  Other labs such as an A1C, thyroid panel, LFTs, cholesterol and triglycerides can also be grossly abnormal.
Initial management: 
  • Fluids.  Start two large bore IVs and start NS.  Patients may be severely dehydrated, around 5-6%, but it is important not to correct this too quickly.  Osmotic shifts and cerebral edema is a major cause of morbidity and mortality.  1L/hr in adults, 10-20mL/kg in kids is sufficient over the first hour and resuscitation volumes should not exceed 40 to 50 mL/kg during the first 4 hours of treatment, unless the patient is in shock (Olivieri).
  • Potassium.  Hypokalemia is also potentially life-threatening.  They may have high/normal values because of proton exchange due to academia, but these patients are always low.  Once you get your K+ result, decide if you need to replete this prior to starting insulin.  If the K+ is less than 3.0, aggressively replenish this prior to starting insulin which will shift this intracellularly and further lower the blood concentration.  Once over 3.3 mmol/dL, you may start insulin at 0.1units/kg/hr. (No need to bolus insulin).  **Keep in mind that your potassium will not improve if the Mg2+ is low.  Replace this as needed as well.
  • The goal, as everyone knows, is to close the AG. Check the glucose q1h and if < 250-300mg/dL, switch fluids to D5NS while continuing insulin gtt. You may need to increase this to D10NS or lower the insulin to 0.5U/kg/hr to prevent hypoglycemia. The goal should be around 200 while the AG is closing.


  • Hourly neurologic checks, especially in peds, are paramount.  Sign of cerebral edema (headache, blurred vision, confusion, focal neuro deficits, Cushing’s triad, urinary incontinence, hypoxia, AMS), which is nearly exclusive to kids, must be taken seriously. Elevate the head of the bed immediately, slow IVF rate by 1/3, and give mannitol 0.5 to 1 g/kg IV over 20 minutes. You may also consider 3% hypertonic saline at 5-10mL/kg over 30 minutes.

“Cerebral edema is seen in 1% to 5% of patients with DKA, has a high mortality rate (up to 90% is some studies ) with many survivors having longterm neurologic deficits” (Olivieri).

Box 3 – Olivieri
Risk factors for pediatric DKA-induced cerebral edema

  •  New-onset diabetes15
  •  Younger age
  •  Longer duration of DKA symptoms
  •  Degree of acidosis at presentation (pH <7.1)17,41
  •  Greater hypocapnia (PCO2 <20 mm Hg)15,17
  •  Greater initial rate of fluid resuscitation for treatment of severe DKA (>50 mL/kg in the first 4 hours)41
  •  Administration of insulin during the first hour of fluid resuscitation41
  •  Higher blood urea nitrogen at presentation15,75
  •  Slower increase in measured serum sodium concentration during treatment of DKA15,66
  •  Bicarbonate treatment15,73

Case Resolution: 

Lab results: Glucose 665, bicarb 5, K 3.3, pH 7.1, Na 130.

“Sodium concentration should be corrected to account for the dilutional effect of the degree of hyperglycemia. The anion gap, however, is calculated using the measured serum sodium level rather than a corrected sodium level because glucose is electrically neutral and does not contribute to the anion gap.” (Olivieri)  

Na Correction Equation: Serum Na + 1.6 [(serum glucose in mg/dL 100)/100].

NS was started and PICU consulted for admission given severe metabolic disturbance.  No source of infection apparent on initial screen.  She was transferred safely to the unit for further management.

Further references and links to concise summaries:
  1. http://coreem.net/core/dka/
  2. CanadiEM: Is NS the Coke of Crystalloid Fluid?
  3. EMDocs.net: Myths in DKA Management
  4. REBEL EM: Diabetic Ketoacidosis (DKA) Myths
  5. Peds EM Morsels: Cerebral Edema and Diabetic Ketoacidosis

Take Home Points

  • DKA is a common, life-threatening emergency but aggressive, comprehensive care markedly reduces morbidity and mortality
  • DKA should be suspected and rapidly diagnosed in all patients with diabetes who present to the Emergency Department
  • Severe hypokalemia is the most common cause of morbidity and mortality in patients with DKA. Hold insulin until the serum potassium is known and aggressively replete potassium and monitor serum concentrations
  • Always search for the underlying cause of the patient’s DKA presentation keeping in mind that infection is the most common cause.
  • Adults: 1-2L/hr initial fluid resuscitation
  • Pediatrics: 10-20 ml/kg/hr initial fluid resuscitation
  • Replace K prior to starting insulin if < 3.0, start insulin once K >3.3
  • Insulin: NO BOLUS, 0.1 U/kg/hr infusion until gap closes
  • Transition to SQ insulin once gap closes
  • Add glucose to mIVF with level 250-300
  • Watch for signs of cerebral edema…especially in kids!