DKA - EPNO - Emergency Physicians of Northwest Ohio

Report
DKA: Management and Pitfalls
Justin Bright, M.D.
Emergency Physicians of NW Ohio
February 20, 2013
Goals For Today
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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
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BHOB > 5 mEq/L
Blood glucose > 250 mg/dL
pH < 7.3
HCO3 < 18 mEq/L
The Stats
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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?
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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
– 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
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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
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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!
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WBC 14
Na 126
Cl 92
HCO3 8
BUN 30
Cr 1.3
K 3.7
Glucose 786
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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
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ABC’s
IV, O2, Monitor
Fluids
Insulin
Correction of other electrolytes
IV Fluids in DKA
• Start with .9NS
– 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
– 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?
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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?
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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?
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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
– 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!

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