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Hyperglycemic Emergencies Diabetic Ketoacidosis and Hyperosmolar - - PowerPoint PPT Presentation

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Hyperglycemic Emergencies Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State Jordanna Kapeluto and Evelyn Wong PGY-5 Endocrinology June 10/June 28, 2015 J Kapeluto 2015 Learning Objectives Definition and Physiology of Diabetic

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Hyperglycemic Emergencies

Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State

Jordanna Kapeluto and Evelyn Wong PGY-5 Endocrinology June 10/June 28, 2015

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SLIDE 2
  • Definition and Physiology of Diabetic Hyperglycemia

Syndromes

  • Causes of Diabetic Hyperglycemia Syndromes
  • Management of DKA/HSS
  • Special Considerations in DKA

Learning Objectives

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SLIDE 3

Abbr Term Abbr Term DKA Diabetic ketoacidosis Na Sodium HHS Hyperglycemic hyperosmolar state K Potassium AG Anion gap T1DM Type 1 diabetes mellitus AGMA Anion gap metabolic acidosis T2DM Type 2 diabetes mellitus SGLT2 Sodium glucose transporter 2 BUN Blood urea nitrogen Osm Osmolality ECG Electrocardiogram NS Normal saline AXR Abdominal x-ray LBW Lean body weight IVF Intravenous fluids HF-PEF Heart failure with preserved ejection fraction HF-REF Heart failure with reduced ejection fraction u/o Urine output ABG Arterial blood gas

Abbreviations in this session

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Epidemiology

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Fishbein et al. Diabetes in America. 1995. Chiasson et al. CMAJ. 2003.

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DKA HHS Population Type 1 (2/3) Type 2 (1/3) Type 2 Incidence 4.6 – 8.0 per 1000 person-years < 1 per 1000 person-years Morbidity 5000 – 10 000 hospitalizations 500 – 1000 hospitalizations Mortality 4 – 10% Recurrent DKA:  all- cause mortality 30% 10 – 50% Underlying illness

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DKA

  • (Polyuria)
  • (Polydipsia)
  • (Weight loss)
  • Vomiting
  • Volume

depletion

  • Abdominal pain
  • Hyperventilation

Clinical Presentation

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HHS

  • Polyuria
  • Polydipsia
  • Weight loss
  • Volume depletion
  • Neurologic

– Lethargy – Coma – Hemianopsia – Hemiparesis – Seizures

Severity Chronic Acute

DKA

  • ฀skin turgor
  • Dry axillae
  • Dry oral mucosa
  • ฀JVP
  • Tachycardia
  • Hypotension
  • Ketone breath
  • Kussmaul

breathing

Kitabchi A et al. Diab Care. 2009

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Physiology of Hyperglycemia

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Chiasson et al. CMAJ. 2003.

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Diagnosis – Diabetic Ketoacidosis

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Hyperglycemia* Ketones Acidosis

  • AGMA
  • pH < 7.35
  • AG >12
  • +/- ฀lactate
  • Resp alkalosis
  • > 13.9 mmol/L
  • [Euglycemic DKA]
  • Acetoacetic acid
  • Beta-

hydroxybutyric acid

  • Acetone

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+ +

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SLIDE 8

Diagnosis – Diabetic Ketoacidosis

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DKA Mimickers Ketones AGMA

  • Starvation (HCO3 >18)
  • Alcohol
  • Lactic acidosis
  • Toxicities
  • Acute/chronic renal failure

Kitabchi A et al. Diab Care. 2009

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SLIDE 9

Management – Issues

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Ketosis Acidosis

Hyperglycemia

Potassium Underlying Cause Sodium Volume

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SLIDE 10

Management

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Volume

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  • Hyperglycemia ⬆osmotic diuresis ⬆ volume depletion

Step 1 – Volume

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  • Average fluid deficit: 3-6L
  • Replacement:
  • Hemodynamic stability
  • Start with NS (0.9% NaCl)
  • 500-1000 cc/hr (15-20cc/kg/hr)

x 1 hour

  • Full replacement over 24 hours
  • Reassess using JVP/volume

status q1h initially and Na

  • (Dextrose)

Kitabchi A et al. Diab Care. 2009

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SLIDE 12
  • Cerebral edema?

Step 1 – Volume

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  • More common in patients <20 years (0.3-1%)
  • Can occur in adults
  • Mortality 20-40%
  • DKA >>> HHS
  • Pathophysiology unknown
  • Often present prior to therapy
  • First 12-24 hours
  • Monitor: headache  lethargy, decreased arousal  seizures,

incontinence, pupillary changes, bradycardia, and respiratory arrest

Kitabchi A et al. Diab Care. 2009

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  • Prevention of (worsening) cerebral edema

Step 1 – Volume

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  • DKA
  • Cautious fluid replacement
  • 15-20 cc/kg LBW/hr
  • Maximum <50cc/kg in first 2-3

hours

  • Dextrose in IVF once serum

glucose reaches 11.1 mmol/L

  • HHS
  • Same as DKA
  • Add dextrose in IVF to maintain

serum glucose 13.9-16.7 mmol/L

  • Maintain serum glucose until

hyperosmolality improving and mental status/clinically stable

  • Pulmonary edema

– Non-cardiogenic: due to reduction colloid osmotic pressure – Cardiogenic: caution with IVF in oligo/anuric CKD and HF-PEF/HF-REF

Kitabchi A et al. Diab Care. 2009

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SLIDE 14

Monitoring

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6 12 18 24 Time Volume pH Ketones

Kitabchi A et al. Diab Care. 2009

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SLIDE 15

Management

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Volume Potassium

Volume

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  • Insulin deficiency + acidosis ⬆ extra cellular shift K + urinary

losses

  • Total K deficit 3-5 mEq/kg
  • Renal function – u/o 50 cc/hr
  • Monitor q2h initially then q4h, choose venous or ABG
  • PO or central IV if K decreasing with IVF
  • Caution with K replacement in CKD – rarely hypoK

Step 2 - Potassium

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K < 3.3 K 3.4-4.9 K > 5.0-5.2

  • Do not start insulin

until K > 3.3

  • IVF 40 mmol/L
  • IVF 10-40 mmol/L
  • Monitor K

Kitabchi A et al. Diab Care. 2009

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SLIDE 17

Monitoring

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6 12 18 24 Time Volume Potassium pH Ketones

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SLIDE 18

Management

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Volume Insulin

Volume Potassium

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  • Insulin deficiency ฀ hyperglycemia + ketosis
  • Insulin therapy – treating the acidosis NOT hyperglycemia
  • Bolus vs. No bolus

– No benefit to bolus – Theoretical large intracellular shift in potassium

  • Insulin R IV 0.1-0.15 units/kg LBW/hr to start

– Average 70 kg person = 7 units/hr

Step 3 – Insulin

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Kitabchi A et al. Diab Care. 2009

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  • Monitoring insulin therapy in DKA
  • CBG measurements q1h + venous with other electrolytes
  • IVF lowers sugars ฀ can have rapid decrease in glucose within

first hours of treatment

– increased renal perfusion and glycosuria – dilutional effect

  • Do not stop insulin if glucose low – start dextrose (D5 + IVF)

and reduce rate of insulin or give insulin 0.1 units/kg SC q2h

– DKA: CBG 11.1 mmol/L – HHS: CBG 16.7 mmol/L

Step 3 – Insulin

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Kitabchi A et al. Diab Care. 2009

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  • Monitoring acidosis in DKA
  • Calculate the anion gap with each measurement of

electrolytes

  • Bicarbonate

– IV bicarbonate = controversial – pH <6.9 100 mmol sodium bicarbonate (two amps) in 400 cc sterile water + 20 mEq KCI at 200 cc/hr for 2 h – Stop when pH >7.0 – Monitor K

Step 3 – Insulin

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AG = Na – (Cl + HCO3)

Kitabchi A et al. Diab Care. 2009

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SLIDE 22

Monitoring

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6 12 18 24 Time Volume Potassium Glucose

AG orHCO3

pH Ketones

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SLIDE 23

Management

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Volume Sodium

Volume Potassium Insulin

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  • Hyperglycemia + fluid shifts ฀ sodium disturbances

– Hypernatremia = indicates severe volume depletion – Hyponatremia = most common – Pseudohyponatremia = lab artifact/dilutional effect from hyperglycemia

  • Total Na also depleted 7-10 mEq/kg
  • Monitor q2h initially then q4h
  • Adjust IVF from NS to 1/2 NS if overcorrecting hypoNa

Step 4 – Sodium

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Correction calculation: +3 mmol/L Na for every 10 mmmol/L of glucose above 10

Kitabchi A et al. Diab Care. 2009

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Monitoring

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6 12 18 24 Time Volume Potassium Glucose Sodium

AG orHCO3

pH Ketones

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SLIDE 26

Management

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Volume Precipitant

Volume Potassium Insulin Sodium

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Step 5 – Causes of DKA

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Insulin deficiency

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SLIDE 28

Step 5 – Causes of DKA

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Insulin deficiency

  • New T1DM
  • Adherence

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Step 5 – Causes of DKA

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Insulin deficiency

  • New T1DM
  • Adherence
  • (C-peptide levels)

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Step 5 – Causes of DKA

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Iatrogenic

  • (C-peptide levels)

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Step 5 – Causes of DKA

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Iatrogenic

  • Medications
  • Glucocorticoids
  • (C-peptide levels)

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Step 5 – Causes of DKA

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Iatrogenic

  • Medications
  • Glucocorticoids
  • (C-peptide levels)
  • Thiazide diuretics
  • Sympathomimetics
  • Lithium
  • Cocaine
  • Atypical antipsychotics
  • Fluoroquinolones
  • Prednisone
  • Dexamethasone
  • Hydrocortisone

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Step 5 – Causes of DKA

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Iatrogenic

  • Medications
  • Glucocorticoids
  • (C-peptide levels)
  • Urine toxin screen
  • Thiazide diuretics
  • Sympathomimetics
  • Lithium
  • Cocaine
  • Atypical antipsychotics
  • Fluoroquinolones
  • Prednisone
  • Dexamethasone
  • Hydrocortisone

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SLIDE 34

Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen

Infection

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  • Bacterial > viral >

fungal

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Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen

Infection

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  • Bacterial > viral >

fungal ICU Setting (n=40) Type:

  • 1. Urinary
  • 2. Gastrointestinal

Pathogens:

  • 1. E. coli
  • 2. Staph aureus
  • 3. Klebsiella pneumoniae

Azoulay E et al. Clin Infect Dis. 2001

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SLIDE 36

Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen
  • Blood cultures
  • Urine cultures
  • Respiratory cultures
  • Wound/Bone biopsy

Infection

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  • Bacterial > viral >

fungal ICU Setting (n=40) Type:

  • 1. Urinary
  • 2. Gastrointestinal

Pathogens:

  • 1. E. coli
  • 2. Staph aureus
  • 3. Klebsiella pneumoniae

Azoulay E et al. Clin Infect Dis. 2001

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Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen
  • Blood cultures
  • Urine cultures
  • Respiratory cultures
  • Wound/Bone biopsy

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Intoxication

  • Alcohols*
  • Illicit drugs
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Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen
  • Blood cultures
  • Urine cultures
  • Respiratory cultures
  • Wound/Bone biopsy
  • Serum osmolality, Na,

glucose, BUN

  • Lactate

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Intoxication

  • Alcohols*
  • Illicit drugs
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Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen
  • Blood cultures
  • Urine cultures
  • Respiratory cultures
  • Wound/Bone biopsy
  • Serum osmolality, Na,

glucose, BUN

  • Lactate

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Ischemia

  • Myocardial
  • Stroke
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SLIDE 40

Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen
  • Blood cultures
  • Urine cultures
  • Respiratory cultures
  • Wound/Bone biopsy
  • Serum osmolality, Na,

glucose, BUN

  • Lactate

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Ischemia

  • Myocardial*
  • Stroke

Hypoglycemia Myocardial Infarction DKA

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Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen
  • Blood cultures
  • Urine cultures
  • Respiratory cultures
  • Wound/Bone biopsy
  • Serum osmolality, Na,

glucose, BUN

  • Lactate
  • Troponin, ECG

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Ischemia

  • Myocardial
  • Stroke
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Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen
  • Blood cultures
  • Urine cultures
  • Respiratory cultures
  • Wound/Bone biopsy
  • Serum osmolality, Na,

glucose, BUN

  • Lactate
  • Troponin, ECG

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Intra-abdominal

  • Pancreatitis
  • Ischemic bowel
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Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen
  • Blood cultures
  • Urine cultures
  • Respiratory cultures
  • Wound/Bone biopsy
  • Serum osmolality, Na,

glucose, BUN

  • Lactate
  • Troponin, ECG
  • Lipase or amylase
  • AXR/Ultrasound/CT

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Intra-abdominal

  • Pancreatitis
  • Ischemic bowel
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SLIDE 44

Step 5 – Causes of DKA

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  • (C-peptide levels)
  • Urine toxin screen
  • Blood cultures
  • Urine cultures
  • Respiratory cultures
  • Wound/Bone biopsy
  • Serum osmolality, Na,

glucose, BUN

  • Lactate
  • Troponin, ECG
  • Lipase or amylase
  • AXR/Ultrasound/CT

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Idiopathic

  • Unidentified cause
  • Psychological
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Monitoring

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6 12 18 24 Time Volume Potassium Glucose Sodium Causes Of DKA Lactate Troponin Cr/BUN pH Ketones

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Management

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Volume Transition

Volume Potassium Insulin Sodium Precipitant

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  • Can start transition when:

– Blood glucose ~ 11.1 mmol/L or less – Plus two of:

  • Anion gap closed (AG <12)
  • Serum bicarbonate > 15 mmol/L
  • pH >7.3

– Patient alert – Patient able to tolerate oral intake – At meal time (breakfast or dinner > lunch)

Step 6 – Transitioning to Subcutaneous Insulin

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Kitabchi A et al. Diab Care. 2009

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SLIDE 48
  • Estimated dose: 0.5-0.8

units/kg/day

  • TDD ÷ 6
  • 3x (1/2 TDD) given as basal

insulin

  • 1x (1/6 TDD) given as

prandial insulin

Step 6 – Transitioning to Subcutaneous Insulin

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  • How to dose insulin during a transition for DKA
  • Involve Endocrinology team early

New Diagnosis T1DM

  • Restart basal insulin at

previous dose

  • Restart prandial insulin +/-

sliding scale

Known Diagnosis T1DM Known Diagnosis T2DM

  • Estimated basal insulin 0.3

units/kg/day

  • Consider restarting oral

agents

Kitabchi A et al. Diab Care. 2009

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SLIDE 49

Monitoring

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6 12 18 24 Time Volume Potassium Glucose Sodium Causes Of DKA

AG orHCO3

Lactate Troponin Cr/BUN pH Ketones pH >7.3 AG <12 CBG 11.1 HCO3 >15

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SLIDE 50

Precipitant

Management

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Volume Prevention

Volume Potassium Insulin Sodium Transition

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SLIDE 51
  • How a healthcare provider can prevent future episodes of

DKA or HHS: – Early contact with a health care provider (Endo, RN, GP) – Sick day management strategies

  • Frequent testing of glucose, ketone checks if CBG >15
  • Maintaining basal insulin use
  • Ongoing fluid/ carb intake
  • Contact health care provider if ketones, inability to keep fluids

down

– Adequate supervision and staff education in long-term facilities

Step 7 – Prevention

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Kitabchi A et al. Diab Care. 2009

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SLIDE 52

Diagnosis and Management

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DKA HHS

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Diagnosis – Hyperosmolar Hyperglycemia State

34 DKA HHS Mild Moderate Severe Plasma glucose (mmol/L) >13.9 >13.9 >13.9 >33.3 Arterial pH 7.25-7.30 7.00-7.24 <7.00 >7.30 Serum bicarbonate (mEq/L) 15-18 10-<15 <10 <18 Urine ketones Positive Positive Positive Small Serum ketones Positive Positive Positive ≤ Small Serum ketones 3-4 mmol/L* 4-8mmol/L >8 mmol/L <0.6 mmol/L* Serum osmolality Variable Variable Variable Variable Anion gap >10 >12 >12 Variable Level of consciousness Alert Alert/drowsy Stupor/coma Stupor/coma

Kitabchi et al. Diab Care. 2009

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HHS Diagnosis:

  • serum glucose >33.3 mmol/L
  • arterial pH >7.3
  • serum bicarbonate >15 mEq/L
  • minimal ketonuria and ketonemia
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SLIDE 54
  • Some differences between HHS and DKA

Management – HHS

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Volume Potassium Insulin Precipitant Sodium Transition Fluid deficit 6-10L Less concern cerebral edema Caution as patients more likely to have AKI/CKD May require higher doses More insulin resistance Chronic process Caution with correction More likely hyperNa Patients tend to older and more sick More comorbidities May involve oral agents

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  • T1DM = autoimmune process
  • Higher rate of other autoimmune conditions in T1DM:

– Celiac disease – Grave’s disease/Hashimoto’s thyroiditis – Primary adrenal insufficiency (Addison’s) – Polyglandular autoimmune syndrome (Schmidt’s)

  • If patient with DKA remains hypotensive/hemodynamically

unstable despite fluids/treatment ฀ CONSIDER ADRENAL INSUFFICIENCY

– Glucocorticoid replacement: hydrocortisone 100mg IV q8h

Special Considerations in DKA

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SLIDE 56
  • Euglycemic DKA

– (+) ketones – AGMA – Blood glucose “normal”  <13.9 mmol/L

  • Occurring in T1DM and T2DM patients on SGLT2 inhibitors

– Canagliflozin (Invokana) – Dapagliflozin (Farxiga)

  • Check ketones, bicarbonate, AG in patients taking these

medications if unexplained nausea/vomiting or altered LOC with relatively normal CBG

Euglycemic DKA

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SLIDE 57

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DKA management pearls – C Yu 2013

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SLIDE 58
  • Kitabchi A et al. Hyperglycemic Crises in Adult

Patients With Diabetes. Diabetes Care. July 2009; 32( 7): 1335-1343

  • Chiasson JL et al. Diagnosis and treatment of diabetic

ketoacidosis and the hyperglycemic hyperosmolar

  • state. CMAJ. April 2003; 168(7): 859-866

Resources

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SLIDE 59

Questions?

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