Surviving DKA (as house staff) Matt Bouchonville Endocrinology Division Thursday School July 25,...
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![Page 1: Surviving DKA (as house staff) Matt Bouchonville Endocrinology Division Thursday School July 25, 2013.](https://reader036.fdocuments.us/reader036/viewer/2022062718/56649e7e5503460f94b80dfb/html5/thumbnails/1.jpg)
Surviving DKA(as house staff)
Matt Bouchonville
Endocrinology Division
Thursday School
July 25, 2013
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↓ insulin↑
counterregulatory hormones
DKA+ =
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Hyperglycemia
Ketosis Acidosis
DKA
↓ insulin ↑ glucagon
↑ gluconeogenesis
↓ glucose utilization
↑ lipolysis
↑ ketone bodies
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↓ insulin
↑ glucagon↑ GH↑ cortisol↑ catecholamines
↑ lipase
Adipocytes
↑ glycerol ↑ FFA
gluconeogenesis ketoacids(acetoacetic acid,
betahydroxy butyrate)
Liver
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DKA
HHS
Absolute InsulinDeficiency
Relative InsulinDeficiency
↑ CounterregulatoryHormones
↑ Ketoacidosis Absent or minimalketogenesis
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DKA on the rise
http://www.cdc.gov/diabetes
2009: 140,000 admissions for DKA
~10% of all diabetes-related admissions
Dis
char
ges
(in
Th
ou
san
ds)
Year
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DKA: Mortality rates stable
http://www.cdc.gov/diabetes
YearYear
Nu
mb
er
Rat
e (p
er 1
00,0
00)
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DKA: Mortality rates stable
http://www.cdc.gov/diabetes Mortality (%)
Ag
e g
rou
p (
yrs)
2006 – Overall mortality rate for DKA: 0.41%
• Mortality:– Precipitating event-related– DKA-related
• Hyperglycemia osmotic diuresis dehydration shock• Acidosis electrolyte imbalance arrhythmias
impaired cardiac contractility shock
vasodilation shock
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Objectives
• Diagnosis
• Management
• Common “Pitfalls”
• Clinical cases
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Diabetes Care, Vol 32 (7)1335-1343, 2009
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Diagnosis of DKA
• Physical Exam
• Tachycardia
• Postural hypotension
• Kussmaul respirations
• Fruity breath
• Altered sensorium
• Abdominal tenderness
• Clinical presentation
• Polydipsia/polyuria
• Constitutional symptoms
• Nausea/vomiting
• Abdominal pain (40-75%)
• Altered sensorium
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Diagnostic Criteria
Diagnostic criteria
Laboratory Parameters
Serum glucose, mg/dL > 250
Arterial pH < 7.3
Bicarbonate, mEq/L <18
Ketones (urine, serum) +
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DKA Severity
Mild Moderate Severe
Laboratory Parameters
Serum glucose, mg/dL > 250 >250 >250
Arterial pH 7.25-7.30 7.00-7.24 <7.00
Bicarbonate, mEq/L 15-18 10-14 <10
Ketones (urine, serum) + + +
Anion gap ↑ ↑ ↑
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Electrolytes and HydrationSerum Total body deficit
Total Water, L n/a 5-8
Laboratory Parameters
Na, mEq/kg ↓(↑↔) 7-10
Cl, mEq/kg 3-5
K, mEq/kg ↑ (↓↔) 3-5
Phos, mEq/kg 5-7
Mg, mEq/kg 1-2
Ca, mEq/kg 1-2
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The Usual Suspects
Factors Precipitating DKA
Most Common Other
Infection (UTI, PNA) Myocardial infarction
Noncompliance Stroke
New-onset diabetes Trauma
Pregnancy
Pancreatitis
EtOH abuse
Medications
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Objectives
• Diagnosis
• Management
• Common “Pitfalls”
• Clinical cases
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Management of DKA
IV Fluids
Assess need forbicarbonate
Insulin Potassium? ? ?
?
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Management of DKA
IV Fluids
Assess need forbicarbonate
Insulin Potassium
Severe dehydration
ShockMild dehydration
0.9% NaCl 1L/hrPressorsCalculate
corrected Na
Na lowNa high Na normal
0.9% NaCl 250-500 cc/hr0.45% NaCl
250-500 cc/hrChange to D5 0.45% NaCl
150-250 cc/hr when glucose reaches 200 mg/dL
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Insulin
IV Bolus: 0.1 U/kg regular
IV Continuous infusion: 0.1
U/kg/hr
If serum glucose does not fall by 50-70 mg/dL in
first hour, double IV rate
Serum glucose ↓ to 200 mg/dL: decrease IV rate
to 0.05-0.1 U/kg/hr
Target glucose: 150-200 mg/dL until DKA resolved
+/-
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Potassium
Establish adequate renal function (UOP
~50 cc/hr)
Serum K+ 3.4-5.2 mEq/L: Give 20-30 mEq K+ in each liter of
IV fluid to maintain serum K+ 4-5 mEq/L
Serum K+ ≤ 3.3 mEq/L: Hold insulin & give 20-30 mEq/hr K+ until serum K+ >
3.3 mEq/L
Serum K+ ≥ 5.3 mEq/L: Do not
give K+ but check serum K+
every 2 hrs
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Assess need for bicarbonate
pH < 6.9 pH 6.9 - 7 pH > 7.0
No HCO3Dilute NaHCO3 (50 mmol) in 200 ml water
with 10 mEq KCl. Infuse 1 hr
Dilute NaHCO3 (100 mmol) in 400 ml water
with 20 mEq KCl. Infuse 2 hr
Repeat NaHCO3 infusion every 2 hr until pH > 7.0. Monitor K+
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Criteria for resolution of DKA
• Serum glucose < 200 mg/dL
• pH < 7.3• Anion gap < 14• Serum bicarbonate ≥ 18 mEq/L
• Ready for transition to SQ insulin?
• Eating >50% meal?
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Transition from IV to SQ insulin• Total daily dose:
• Resume previous outpatient dose• Insulin naïve (new diagnosis of T1D)
• Weight based or infusion rate derived?
• 0.5-0.8 units/kg/day
½ basal
½ bolus
• Timing of SQ insulin dose? 1-2 hours before stopping IV insulin
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Objectives
• Diagnosis
• Management
• Common “Pitfalls”
• Clinical cases
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• Hypoglycemia (10-25%)• Hypokalemia
• Hyperchloremic (nongap) acidosis• NaCl treatment• Loss of substrate for bicarbonate regeneration
• Recurrent DKA• Failure to overlap SQ insulin with IV insulin
Common Pitfalls
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(Less) Common Pitfalls
• Cerebral edema• Associated with rapid correction of serum osmolality• 1% of children with DKA• Reported in young adults• Mortality 40-90%• Clinical manifestations:
• Lethargy• Seizures• Bradycardia• Respiratory arrest
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Objectives
• Diagnosis
• Management
• Common “Pitfalls”
• Clinical cases
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Case #1
• 34 yo F with T1D treated with glargine and humalog presents to ER in DKA. Which of the following antihypertensive medications may be precipitating her current presentation?
A) Lisinopril
B) HCTZ
C) Amlodipine
D) Losartan
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Answer: B) HCTZ
• Medications which may precipitate DKA:• HCTZ• Beta blockers• Steroids• Phenytoin
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Case #2
• 56 yo obese M with T2D treated with metformin, HTN treated with HCTZ, lisinopril brought in by EMS. Obtunded and found to have the following labs:
• Gluc 286 mg/dL
• Creat 3.5 mg/dL
• Bicarb 8 mEq/L
• Anion gap 20
• Serum ketones neg
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Case #2
• What is the most likely cause of this patient’s presentation?
A) DKA
B) HCTZ use
C) Metformin use
D) Vitamin D deficiency
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Answer: C) Metformin use
• Differential diagnosis:• Starvation ketosis
• Generally not hyperglycemic
• Alcoholic ketoacidosis• Bicarb rarely < 18; generally not hyperglycemic
• Anion gap acidosis• Lactic acidosis, salicylates, toxic alcohols
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Case #3
• 29 yo M presents to ER with abdominal pain, nausea, vomiting, weight loss, and polyuria. Found to be in DKA with likely new dx T1D. Hemodynamically stable. Exam remarkable for abdominal tenderness, no peritoneal signs. Labs remarkable for an elevated serum amylase. What next step would be most appropriate to determine whether the patient has acute pancreatitis?
A) CT abdomen
B) Abdominal ultrasound
C) Serum lipase
D) Whipple procedure
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Answer: C) Serum lipase
• Serum amylase levels commonly elevated in patients with DKA (up to 80% cases)
• Lipase much less commonly elevated
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Case #4
• 17 yo F with T1D, poor compliance, admitted with DKA. Treated with aggressive IV fluids, IV insulin. Receives supplemental potassium, phosphate, and magnesium overnight. Presents with tetany in the morning. Which laboratory abnormality could explain this finding?
A) Serum potassium
B) Serum phosphate
C) Serum magnesium
D) Serum calcium
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Answer: D) Serum calcium
• Phosphate replacement:• Prospective randomized studies have failed to show
benefit in DKA outcomes• Risk of severe hypocalcemia (younger patients) • Not routinely recommended• ADA: “Careful phosphate replacement may sometimes
be indicated in patients with cardiac dysfunction, anemia, or respiratory depression and in those with a serum phosphate concentration of < 1.0 mg/dL”
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Case #5
• 28 yo M with unknown medical history is brought in by EMS after being found down. The patient is obtunded and found to be in DKA. Serum glucose is 400 mg/dL, serum bicarbonate is 10 mEq/L, anion gap is 20, serum osmolality is 298, serum ketones are positive. Which answer most accurately describes his mental status?
A) It is likely related to the DKA and should improve with treatment
B) It is unlikely to be related to the DKA
C) Both, A & B are correct
D) Answer A
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Answer: B) Unlikely related
• ADA:• “The occurrence of stupor or coma in diabetic patients
in the absence of definitive elevation of effective osmolality (320 mOsm/kg) demands immediate consideration of other causes of mental status change.”
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Objectives
• Diagnosis
• Management
• Common “Pitfalls”
• Clinical cases
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Questions?