1. DKA: Management and Pitfalls
Justin Bright, M.D.
Emergency Physicians of NW Ohio
February 20, 2013

2. Goals For Today Definitions and characteristics of DKA
Appropriate workup
Treatment modalities
Identify pitfalls and complications
Discuss difference in adult vs. pediatric population
Management of DKA here at Henry Ford

3. What Is DKA?
State of insulin deficiency (absolute or relative) causing dehydration, acidosis, and metabolic derangement
By blood work
Anion gap metabolic acidosis
BHOB > 5 mEq/L
Blood glucose > 250 mg/dL
pH < 7.3
HCO3 < 18 mEq/L

4. The Stats DKA is reason for 50% of diabetic admissions
Tends to occur in patients less than 19 yo
Type 1 DM > Type 2 DM
Death occurs in 2% of presenting patients

5. Causes of DKA? Underlying Infection (40%)
Non-compliance with insulin regimen (25%)
New onset diabetes (15%)
Medical or surgical stress (20%)
AMI
Sepsis
“weak and dizzy”
Syncope
Altered mental status

6. What Is Insulin? Anabolic regulatory hormone
Released by pancreas (or administered as supplemental medication) in response to elevated blood sugar
Causes blood sugar to be utilized for fuel, with excess stored as muscle and fat
Inhibits release of glucagon
Inhibits gluconeogenesis and glycogenolysis

7. Pathophysiology Insulin deficiency
Hepatic gluconeogenesis and glycogenolysis
Fatty acid break down  ketogenesis
Byproducts: ketones (acetone, BHOB, acetoacetate)
Excess blood glucose  osmotic diuresis
BHOB induces vomiting  more dehydration
Rising acidosis  potassium shift and osmotic loss

9. What Does DKA Look Like? Insidious onset Weakness, fatigue, malaise
Polydypsia, polyuria
Weakness, fatigue, malaise
Abdominal pain and vomiting as BOHB increases
Altered level of consciousness
May present with symptoms of their concurrent illness that triggered DKA

11. A Case 19 yo female in Room 115.5 Known Hx of diabetes
CC: “One Touch Hi”
Reports being out of her insulin x 1 week
Mother reports patient is more confused and has been vomiting for 2 days

12. What Do You Want To Know?

13. ROS & PE Review of Systems Physical Exam Confusion Vomiting
Frequent urination
LMP 5 weeks ago
Systems otherwise neg
Physical Exam
Tc 37.2, HR 115, BP 108/50, RR 28, SaO2 98
Patient appears pale
Tachypneic, but not in distress
Poor skin turgor and capillary refill
No focal deficits, A/O x 3, but intermittently sleepy during questioning

14. What Should We Order? Diagnostics Therapeutics One touch CBC Lytes
UA, urine preg
ABG w/ lactate
Serum Osm
B-Hob
LFTs
Lipase
EKG
?? Imaging
Therapeutics
IVF Fluids (how much?)
Insulin (how much? Do you want to wait?)
Other meds?

15. Labs Are Back! WBC 14 Na 126 Cl 92 HCO3 8 BUN 30 Cr 1.3 K 3.7
Glucose 786
pH 7.12
CO2 23
Lactate 4.2
B-Hob 6.2
Osm 306
Gap 26
UA: large ketones and glucose
Ucg neg

16. What Do You Think Of The Labs?
Na of 126 corrected  137
K 3.7 (actually much lower intracellularly)
ABG  anion gap metabolic acidosis with incomplete respiratory compensation
Acute kidney injury (pre-renal dehydration)
Lots of serum B-Hob  persistent vomiting

17. So Now What Do We Do?

18. Treatment of DKA ABC’s IV, O2, Monitor Fluids Insulin
Correction of other electrolytes

19. IV Fluids in DKA Start with .9NS Change to ½ NS
If hypotensive  rapid infusion of .9NS until SBP > 80
If normotensive  1L of .9NS in first 30 minutes, another 1L within subsequent 1 hour
Change to ½ NS
Start at 250 cc/hr and titrate to urine output of 1-2 ml/kg/hr
Change to D5 ½ NS when blood sugar is < 250 but hydration still needed

20. Saline vs. Ringers
Must really think about patient’s electrolyte status and composition of the fluids you’re giving
Normal Saline  154 mmol/L Na; 154 mmol/L Cl-
Chloride can contribute to worsening acidosis
½ NS has 77 mmol/L
Ringers  130 mmol/L Na; 109 mmol/L of Cl
Less Cl to contribute to acidosis
LR also promotes HCO3 formation  helps further counter acidosis

21. Insulin Administration
Use regular (Novalin) Insulin  IV
Bolus of 10U IV prior to drip is controversial
Insulin Drip
0.1 U/kg/hr
Stop the drip when blood glucose is 250 or lower
Goal drop in glucose is per hr

22. Electrolytes Potassium Sodium Bicarb Need to watch the K levels!!!!
Patient’s are relatively K depleted
Insulin dramatically reduces K levels
Sodium
Remember that Na levels are deceptive because they are skewed by glucose levels
Bicarb
Use is controversial
Generally not indicated with pH > 7.0
In peds patients  use is associated with higher incidence of cerebral edema

23. More on Potassium Beware of the “warning colors” on Careplus
If K > 6  don’t give more
If K  consider 10 mEq infusion with fluids
If K  give 20 mEq infusion with fluids
If K < 3  give K before giving insulin

24. Why Do DKA Patients Die?

25. Because We Kill Them!

26. How Do We Kill DKA Patients?
Cerebral Edema
Poor ventilator management
Not respecting the K levels
Not monitoring glucose levels enough
CHF from over-aggressive fluid administration

27. Cerebral Edema in DKA Occurs almost exclusively in patients < 20 yo
Mortality approaches 40%
Correlation with HCO3 administration
Causes paradoxical cerebral acidosis as lipid soluble CO2 crosses blood-brain barrier
Initial symptom is headache
Onset hrs from treatment onset
Rapid deterioration of mental status

29. What Do You About It? Manage airway Immediate head CT
Neurosurg consult
Do whatever you can to prevent herniation
mannitol
Pray!

30. Ventilator Management
Must communicate with the RT about vent settings!
Keep in mind patient’s metabolic status
If RR set to low  will develop worsening acidosis
Must try to set RR to match their natural compensatory mechanisms

31. How Do We Prevent Electrolyte Catastrophes?
Hourly one touches
Frequent rechecks of lytes and ABG
Utilize the DKA protocol tab on our order set

32. Disposition In a perfect world  all patients go to MICU In our world
Boarding patients for excessive periods of time
May do a much larger portion of the acute/critical management than in other EDs
How do we know who can go to floor?
Closure of anion gap
Persistent glycemic control
K corrected
Mental status normal
Tolerating PO

33. Pediatric Considerations
Literature suggests 10 cc/kg boluses instead of 20 cc/kg
Cerebral edema is more likely to occur
More likely to have DKA as initial presentation of their diabetes

34. Milwaukee Formula 1st hour 2nd hr – resolution
10 – 20 cc/kg bolus of NS
Monitor neuro status
Insulin drip U/kg/hr
2nd hr – resolution
½ NS (85 ml/kg + maintenance) – initial bolus over next 23 hrs
Continue insulin drip until BS < 250
Potassium supplementation

35. Moral of the Story You will see a lot of DKA patients at HF
You may be in charge of their management for a long period of time
You don’t have to rapidly correct the metabolic derangements
Beware of changes in glucose and K levels
Fear cerebral edema
Beware of ventilator induced death

36. Questions/Comments?
Thank You!