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

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

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

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

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

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

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

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

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

What Do You Want To Know?

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

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?

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

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

So Now What Do We Do?

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

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

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

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 50-100 per hr

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

More on Potassium Beware of the “warning colors” on Careplus If K > 6  don’t give more If K 4.5-6  consider 10 mEq infusion with fluids If K 3-4.5  give 20 mEq infusion with fluids If K < 3  give K before giving insulin

Why Do DKA Patients Die?

Because We Kill Them!

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

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 12-24 hrs from treatment onset Rapid deterioration of mental status

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

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

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

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

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

Milwaukee Formula 1st hour 2nd hr – resolution 10 – 20 cc/kg bolus of NS Monitor neuro status Insulin drip 0.05-0.1 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

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

Questions/Comments? Thank You!