Surviving DKA(as house staff)

Matt Bouchonville

Endocrinology DivisionThursday School

July 25, 2013

↓ insulin ↑ counterregulatory

hormones

DKA+ =

Hyperglycemia

Ketosis Acidosis

DKA

↓ insulin ↑ glucagon

↑ gluconeogenesis↓ glucose utilization

↑ lipolysis

↑ ketone bodies

↓ insulin

↑ glucagon↑ GH↑ cortisol↑ catecholamines

↑ lipase

Adipocytes

↑ glycerol ↑ FFA

gluconeogenesis ketoacids(acetoacetic acid,

betahydroxy butyrate)

Liver

DKA

HHS

Absolute InsulinDeficiency

Relative InsulinDeficiency

↑ CounterregulatoryHormones

↑ Ketoacidosis Absent or minimalketogenesis

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 T

hous

ands

)

Year

DKA: Mortality rates stable

http://www.cdc.gov/diabetes

YearYear

Num

ber

Rat

e (p

er 1

00,0

00)

DKA: Mortality rates stable

http://www.cdc.gov/diabetes Mortality (%)

Age

gro

up (y

rs)

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

Objectives

• Diagnosis

• Management

• Common “Pitfalls”

• Clinical cases

Diabetes Care, Vol 32 (7)1335-1343, 2009

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

Diagnostic Criteria

Diagnostic criteria

Laboratory Parameters

Serum glucose, mg/dL > 250

Arterial pH < 7.3

Bicarbonate, mEq/L <18

Ketones (urine, serum) +

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 ↑ ↑ ↑

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

The Usual SuspectsFactors Precipitating DKA

Most Common Other

Infection (UTI, PNA) Myocardial infarction

Noncompliance Stroke

New-onset diabetes Trauma

Pregnancy

Pancreatitis

EtOH abuse

Medications

Objectives

• Diagnosis

• Management

• Common “Pitfalls”

• Clinical cases

Management of DKA

IV Fluids

Assess need forbicarbonate

Insulin Potassium? ? ?

?

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

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

+/-

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

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+

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?

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

Objectives

• Diagnosis

• Management

• Common “Pitfalls”

• Clinical cases

• 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

(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

Objectives

• Diagnosis

• Management

• Common “Pitfalls”

• Clinical cases

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) LisinoprilB) HCTZC) AmlodipineD) Losartan

Answer: B) HCTZ

• Medications which may precipitate DKA:• HCTZ• Beta blockers• Steroids• Phenytoin

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

Case #2

• What is the most likely cause of this patient’s presentation?

A) DKAB) HCTZ useC) Metformin useD) Vitamin D deficiency

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

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 abdomenB) Abdominal ultrasoundC) Serum lipaseD) Whipple procedure

Answer: C) Serum lipase

• Serum amylase levels commonly elevated in patients with DKA (up to 80% cases)

• Lipase much less commonly elevated

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 potassiumB) Serum phosphateC) Serum magnesiumD) Serum calcium

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”

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

treatmentB) It is unlikely to be related to the DKAC) Both, A & B are correctD) Answer A

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.”

Objectives

• Diagnosis

• Management

• Common “Pitfalls”

• Clinical cases

Questions?