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DKA: Management and Pitfalls

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Presentation on theme: "DKA: Management and Pitfalls"— Presentation transcript:

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!

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