Diabetic Emergencies Flashcards

1
Q

Consequences of diabetic emergencies

A

Blindness
Renal failure
Amputation
Heart disease (basically inevitable)
Stroke

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2
Q

What does being Hyperglycemic for long periods of time increase risks of? why?

A

Infection
MI
PE
CVA
DVT

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3
Q

Bodily functions that happen when someone is Hyperglycemic for long periods of time

A

Clotting
Vasoconstriction
Impaired gastric motility
Decreased respiratory muscle function

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4
Q

*Target goals of blood sugar for patient with hyperglycemia in ICU

A

Initially: less than or equal to 180
Then *140-180

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5
Q

Why aren’t targets of less than or equal to 110 recommended?

A

May be associated with increased mortality

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6
Q

What is glucose metabolism regulated by?

A

Regulated by the liver

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7
Q

How does the liver regulate glucose metabolism?

A

Liver stores and synthesizes glucose (stored as glycogen)

Liver releases glucose when BS decreases
Liver stores glucose when BS increases

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8
Q

How is glucose stored?

A

In the liver as glycogen
In skeletal muscle as glycogen
In fat cells as triglycerides

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9
Q

What does insulin stimulate?

A

Glucose uptake by cells
Synthesis of glycogen
Synthesis off protein and amino acids
Transport of amino acids and fatty acids into cells
Conversion of fatty acids to triglycerides

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10
Q

What does insulin inhibit?

A

Glucose production (by glycogenolysis and glyconeogenesis)
Lipolysis
Protein catabolism

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11
Q

What is glycogenolysis?

A

Breakdown of glycogen into glucose to be used

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12
Q

What is gluconeogenesis?

A

Production of glucose from proteins/fat

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13
Q

What is the body’s physiologic response to insufficient insulin?

A

Decreased glycogenesis (glucose stays in bloodstream)
Increased glycogenolysis (but not enough insulin to actually use, so it stays in blood)
Increased gluconeogenesis
Decreased glycolysis
Increased Lipolysis

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14
Q

What is glycolysis?

A

Breakdown of glucose to CO2 and H2O

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15
Q

What is Lipolysis?

A

Breakdown of fats to ketones, an alternative energy source

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16
Q

What are the 5 counterregulatory hormones?

A

Glucagon
Epinephrine
Cortisol
Norepinephrine
Growth hormone

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17
Q

*What do the counterregulatory hormones do?

A

*Increase blood glucose

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18
Q

What causes a Hyperglycemic crisis (DKA or HHS)?

A

Result from reduction in net effect of circulating insulin
Coupled with simultaneous elevation of counter-regulatory hormones
Results in hepatic and renal glucose production and decreased use of glucose in peripheral tissues

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19
Q

*Common factors leading to DKA/HHS

A

Omission of adequate treatment of DM
New-onset DM
Infection
Pre-existing illness
Acute illness
Stress
Other endocrine disorders
High-calorie parenteral/enteral nutrition

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20
Q

Description of DKA

A

Acute complication of DM
Associated with insulin deficiency, coupled with simultaneous increase in counterregulatory hormones

*Results in hyperglycemia, dehydration, electrolyte depletion, and ketones

*Develops quickly

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21
Q

S/S of DKA

A

Hyperglycemia
Dehydration
Electrolyte depletion
Ketosis

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22
Q

Contributing factors of DKA

A

Insulin pump malfunction
Insulin pump infusion set/site issues
Increased insulin need

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23
Q

What could be the causes of insulin pump infusion set/site issues?

A

Infection
Disconnection
Catheter kink/migration

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24
Q

What could cause increased insulin need?

A

Insulin resistance due to:
Pregnancy
Puberty
Before menstruation

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25
Q

Clinical manifestations of DKA

A

Classic S/S: Polyuria, polydipsia, polyphagia, hot dry skin
Cardiovascular: Dehydration, electrolyte imbalances, Tachycardia, hypotension, Weak, thready pulse
GI: Anorexia, nausea, vomiting, abdominal pain, weight loss (r/t decreased blood volume from loss of fluid)
Neuro: Lethargy, fatigue, altered LOC
Respiratory: Fruity breath, Kussmaul respirations

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26
Q

*Blood glucose measurement for DKA

A

> 250mg/dL (but often much higher: average = 675)

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27
Q

Ketone findings for DKA

A

Positive serum and urine ketones

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28
Q

PH for DKA

A

<7.30

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29
Q

*HCO3 for DKA

A

<15 mEq/L

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30
Q

Sodium for DKA

A

May be normal, low, or high

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31
Q

*Potassium for DKA

A

May initially be normal, then high, then low (low b/c insulin also causes potassium to go into cells)

*regardless of what serum potassium says, there is always a total body potassium defecit

32
Q

BUN and creatinine for DKA

A

BUN >20mg/dL
Cr >1.5 mg/dL

33
Q

Serum osmolality for DKA

A

Avg 330 mOsmkg (*measures concentration: higher = more dehydrated)

34
Q

Order of interventions to manage DKA

A

Correct volume depletion
Correct hyperglycemia
Correct electrolyte imbalances

35
Q

*What type of insulin is used to correct hyperglycemia emergencies?

A

Short acting aka regular insulin

36
Q

Description of HHS

A

Hyperosmolar, hyperglycemic state resulting from inadequate insulin secretion *without significant ketosis

Higher than average BG and higher osmolality

*Insidious onset

May be more severe than DKA

37
Q

Patients HHS are more common in

A

Type 2 DM and elderly

38
Q

Possible causes of HHS

A

*Dehydration (diuretics & not replacing fluids, decreased thirst)
*Stressed induced (MI, CVA, infection)
Enteral/parenteral nutrition
MI, CVA
Glucocorticoids (for long periods)
Other drugs

39
Q

Clinical manifestations of HHS

A

Dry skin & mucous membranes
Extreme thirst (OA may not)
Extreme dehydration (Hypotensive, tachycardia)
Neuro: Generalized focal seizures, Reversible hemiparesis, Confusion, Possible coma

40
Q

*BG for HHS

A

> 1000 mg/dL

41
Q

*Osmolality for HHS

A

> 350 mOsm/L

42
Q

pH for HHS

A

> 7.30

43
Q

HCO3 for HHS

A

> 15 mEq/L

44
Q

Ketones for HHS

A

Negative serum and urine ketones

45
Q

Sodium for HHS

A

Varies related to hydration

46
Q

Potassium for HHS

A

Varies related to hydration

47
Q

BUN and creatinine for HHS

A

Elevated

48
Q

Goal for HHS management

A

To complete rehydration and normalize BG in 24-48 hours

49
Q

*Guidelines to treat HHS and DKA

A

*Replace half of estimated fluid deficit in 8 hours
*Replace remainder in next 16 hours

50
Q

Which patients do we need to be even more careful with when replacing fluids?

A

Patients prone to pulmonary edema, such as pts with renal failure or heart failure
Older adults

Need more frequent monitoring during first hour

51
Q

*Exact guidelines for treating patients with fluid volume deficit related to osmotic diuresis secondary to hyperglycemia
(Which type of fluid to use when)

A

1 - Infuse NS 1 liter over first hour (999 mL/hr) as long as pt can tolerate

2 - Change to .45% NS when Na is normal or increased

3 - When BG reaches about 200 mg/dL, D5&1/2NS to prevent hypoglycemia

52
Q

When treating FVD in hyperglycemia, what should fluids do you give after the NS for the first hour?

A
  • Then 10-15 mL/kg/hr if not shocky (monitor VS, LOC, CVP, PAP, I&O qh)
  • If shocky, 20 mL/kg/hr. Once stable, 7.5 mL/kg/hr
  • Monitor for overload (crackles, decreased LOC, increased BP)
53
Q

How do you determine if a patient is not tolerating fluids?

A

S/S
Regain then lose consciousness
Hearing crackles
Bounding pulses
New onset of high hypertension

54
Q

Which electrolytes may need to be replaced after managing FVD in hyperglycemic patients?

A

K
Phos
Mg
Cl

55
Q

*Symptoms of hypokalemia

A

Muscle weakness
Cramps
Abdominal distention
Hypotension
Weak pulses
Broad flat T waves
U wave visible
PVB’s (heart muscle not right, ventricles over compensating)

56
Q

When does insulin and monitoring of ventricles begin?

A

After:
1 - 1st liter of IVF
2 - K > 3.3 mEq/L (20-30 mEq of K added to IVF)
3 - Pt is producing urine

57
Q

*What is the goal for reducing blood glucose?

A

Reduce by 50-75 mg/dL/hr

58
Q

After treating a DKA patient for FVD, how do you begin treatment with insulin? What is the goal?

A

1st: loading dose of regular insulin (0.1 u/kg of ideal body weight)

2nd: regular insulin infusion at 0.1 u/kg/h until pH>7.3 and HCO3 >15 mEq/L

Monitor BG hourly
Pt usually NPO

59
Q

For a DKA patient, when pH and HCO3 goals are reached, what should you decrease insulin by? And what is the target?

A

3rd: decrease by 0.05 u/kg/hr with target of 100-150 mg/dL until acidosis is resolved

Monitor BG hourly
Pt usually NPO

60
Q

Next steps after acidosis is resolved in a patient with DKA and glucose goal is reached:

A

SC insulin 1-2 hrs prior to discontinuation of infusion, when BG < or = to 200 mg/dL and 2 of the following are met:

Venous pH >7.3
HCO3 > 15 mEq/L
Anion gap > or + 12 mEq/L

61
Q

Once glucose goal is reached and pt’s infusion is ready to be discontinued, how often should BG be monitored?

A

Every 6-8 hours

62
Q

When should acidosis be treated with bicarb?

A

If HCO3 is < 7 or pH is <7

63
Q

For a HHS patient, when pH and HCO3 goals are reached, what should you decrease insulin by? And what is the target?

A

Decrease by 0.2-0.5 u/kg/hr when BG 300 mg/dL

With target 200-300 mg/dL

64
Q

When should HHS patients be transitioned to SC insulin?

A

When mental status improves

65
Q

Why are the guidelines different for decreasing insulin and goal BS different between DKA and HHS patients?

A

Blood sugar is usually higher in HHS patients and these patients are usually more dehydrated
So their symptoms will be fixed faster because of this

66
Q

Education for patient and family after hyperglycemic crisis:

A

Education to prevent future episodes:
Hydration
Reporting illness
Reporting BS >250
Reporting inability to keep food or fluids down
Sick day rules
Monitoring A1C levels

67
Q

*Description of hypoglycemia

A

Acute condition in which relative or absolute *excess of insulin results in *BG < 70 mg/dL

68
Q

Causes of hypoglycemia

A

Too much exogenous insulin
Inappropriate site rotation
Absorption variability
Gastroparesis (delayed emptying)
Inadequate intake
Increased energy requirements
Impaired counterregulation (don’t have those 5 hormones)
Hypoglycemic unawareness

69
Q

5 hormones involved in hypoglycemia

A

Glucagon
Epinephrine
Cortisol
Norepinephrine
Growth hormone
(Glucose usage is inhibited in peripheral tissues by epi, cortisol, GH)

70
Q

Symptoms of mild hypoglycemia
And BG level

A

Patient completely alert
Pallor
Diaphoresis
Tachycardia
Palpitations
Hunger or shakiness
BG < 51-70
Patient is able to drink

71
Q

Treatment of mild hypoglycemia

A

10-15g of glucose (carbohydrate) by mouth

72
Q

Symptoms of moderate hypoglycemia
And BG level

A

Patient is conscious, cooperative, and able to swallow safely
Difficulty concentrating
Confusion
Slurred speech
Extreme fatigue
BG < 55 mg/dL
Patient is able to drink

73
Q

Treatment for moderate hypoglycemia

A

20-30 g of glucose (carbohydrate) by mouth

74
Q

Symptoms of severe hypoglycemia
And BG level

A

Patient is uncooperative or unconscious
BG < 54 mg/dL or patient is unable to drink

75
Q

Treatment for severe hypoglycemia

A

With IV access: 50 mL 50% dextrose in water solution (D50W)

Without IV access: 0.5-1 mg glucagon SQ, IV, IM and turn pt on side or observe to avoid potential aspiration from nausea and vomiting side effect

76
Q

Education for pt and family regarding hypoglycemia

A

Prevention of future episodes:
Teach common causes
Do not change brands of insulin
S/S hypoglycemia
Medic alert bracelet
Self BG monitoring
Keep available source of CHO on person at all times
Identifying cause of episode