Hyperglycemic Crises and Inpatient Control of Diabetes Flashcards

1
Q

What is DKA

A

Diabetic Ketoacidosis
Complication in T1 pts
Hyperglycemia + Ketosis + Acidosis

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2
Q

Pathophysiology of DKA

A

Decreased insulin concentration

Increased counterregulatory hormones

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3
Q

Counterregulatory hormones

A

Catecholamines
Cortisol
Glucagon
Growth Hormones

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4
Q

DKA Hyperglycemia from

A

Increased glyconeogenesis
Accelerated glycogenolysis
Impaired glucose utilizaiton

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5
Q

DKA Lipolysis from

A

Insulin deficiency

Counterregulatory hormones

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6
Q

DKA Transient insulin resistance from:

A

Hormone imbalance

Elevated FFA

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7
Q

Increased FFA oxidation in liver leads to

A

Increased ketone bodies (beta-hydroxybutyrate and acetoacetate) which leads to acidosis

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8
Q

DKA symptoms

A
N/V
Ab pain
Polyuria
Polydispsia
Confusion
Fatigue
Fruity odor on breath (ketones)
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9
Q

DKA presentation

A
Elevated glucose
Low arterial pH
Low serum bicarbonate
Elevated anion gap
Decreasing mental status
Decreased sodium
Increased phosphate
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10
Q

Treatment Goals

A

Correct dehydration, hyperglycemia, electrolyte imbalances
ID and correct precipitating factors
Frequent pt monitoring

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11
Q

Treatment Initial Fluid Therapy

A

Initial: Normal Saline 15-20 mL/kg/hr or 1-1.5 L in the first hr

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12
Q

Treatment Maintenance Fluid Therapy

A

1/2 NS at 250-500 mL/kg OR NS at 250-500 mL/hr if low serum Na
Once glucose is ~200 mg/dL –> add 5% dextrose to fluids
Correct fluid deficits within 24 hrs

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13
Q

Treatment Insulin Therapy

A

Initial IV bolus of regular insulin 0.1u/kg
Continuous infusion regular insulin 0.1u/kg/hr
When serum glucose reaches 200, decrease insulin to 0.02-0.05 u/kg/hr
Maintain glucose between 150-200

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14
Q

Treatment Potassium Replacement

A

Replace K+ when levels fall below UNL
20-30 mEq/L fluid maintenance
Goal: 4-5 mEq/L
Delay insulin until K+ is >3.3 bc it pushes it intracellularly

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15
Q

Treatment of Bicarb and Phosphate Replacement

A

Bicarb: pH < 6.90

Phosphate is pushed intracellularly by insulin

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16
Q

Transitioning to SQ insulin

A

Glucose < 200 + 2 of the following:
Bicarb >15
pH >7.3
Anion gap <12

Overlap for 1-2 hrs

17
Q

If insulin naive:

A

Start multi-dose insulin regimen at 0.5-0.8 u/kg/day

18
Q

Cerebral Edema Signs and Symptoms

A
Headache
Level of consciousness deterioration
Seizures
Incontinence
Pupilary changes 
Bradycardia
Decreased BP
19
Q

Prevention of Cerebral Edema

A

Avoid excessive hydration
Avoid rapid reduction in plasma osmolarity
Gradual decrease in serum glucose
Maintain glucose at 250-300 until mental status normalized

20
Q

Treatment of Cerebral Edema

A

Mannitol infusion

Mechanical ventilation

21
Q

What is HHS

A
Hyperglycemic Hyperosmolar Syndrome
Usually from restricted water intake
Days to weeks
Dehydration- osmotic diuresis
Relative insulin deficiency (prevents lipolysis -- no acidosis)
22
Q

Presentation of HHS

A
Hemiparesis and seizures
A lot higher glucose than DKA
Normal pH
Normal bicarb
High osmolarity --> diuresis
Worse mental status
23
Q

Treatment for HHS

A

Fluid therapy: NS or 1/2 NS
Once glucose is ~300 add dextrose
Insulin therapy: Decrease rate when glucose is ~300

24
Q

Challenges to inpatient glycemic control

A

Acute illness
Inconsistent caloric intake
Changes in medications
Limitations in glucose monitoring and insulin administration

25
Q

Goals in Critically Ill Patients

A

Initiate IV insulin when BG >180 mg/dL
BG target = 140-180
Avoid hypoglycemia

26
Q

Goals in Non-critically ill patients

A

Fasting BG <70

27
Q

Management

A

Oral meds may need to be discontinued upon admission

Sliding scale insulin alone is not appropriate for hospitalized patients

28
Q

Management of Critically ill patients

A

Continuous IV insulin is preferred method in this population

29
Q

Management of Non-Critically Ill Patients

A

SQ insulin preferred (basal/bolus)