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[Mine] core curric - 2016 > Ch 17: Complications of Parenteral Nutrition > Flashcards

Ch 17: Complications of Parenteral Nutrition Flashcards

1
Q

Serum triglycerides provide a reasonable estimate of

ASPEN self assessment - PN

A

body lipid clearance

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2
Q

Lipid free PN Rx can cause EFAD within _ _ _ weeks in acutely ill patients
Although physical evidence of deficiency may not be noticed, biochemical deficiencies can be suspected by:

ASPEN self assessment - PN

A
  • within 2 weeks
  • elevated AST, ALT
  • confirmed by triene: tetraene ratio.
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3
Q

Recommended dosage for all types of ILE are _ _ _ g/kg/day.
Lipid dosing should not to exceed _ _ _ g/kg/day

ASPEN self assessment - PN

A

1-2g/kg/day,
not to exceed 2.5g/kg/day

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4
Q

What deficiency exacerbates lipid abnormalities?
Existing evidence has not confirmed that supplementation corrects _ _ _

ASPEN self assessment - PN

A

L-carnitine

hypertriglyceridemia

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5
Q

Most common complication associated with PN

A

Hyperglycemia

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6
Q

Stress associated causes of hyperglycemia

A
  • insulin resistance
  • increased gluconeogenesis and glycogenolysis
  • suppressed insulin secretion
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7
Q

Excess CHO administration →

A
  • hyperglycemia
  • hepatic steatosis
  • increase CO2 production
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8
Q

Target BG levels per ASPEN and SCCM

A
  • ASPEN: 140-180 mg/dL in adult hospitalized patients receiving nutrition support
  • SCCM: 150-180 mg/dL for ICU populations
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9
Q

Insulin therapy in PN

A
  • Initial PN insulin: 0.05 to 0.1 unit/g dextrose OR 0.15 to 0.2 units/g dextrose if already hyperglycemic
  • Only regular insulin should be added to PN bag
  • Do not advance dextrose until BG is controlled
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10
Q

How much of the total amount of SSI required over 24 hours may be added to the next day PN?

A

Two-thirds

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11
Q

Hyperglycemia is associated with worsened clinical outcomes:

A
  • increased risk of infection
  • poor wound healing
  • inability to gain weight
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12
Q

Do not exceed a GIR of _ _ _ from CHO in acutely ill patients

A

4-5 mg/kg/d
(20-25 kcal)

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13
Q

What nutrient deficiency can cause hyperglycemia?

A
  • Rarely, hyperglycemia may be related to chromium deficiency
  • Insulin is less effective in these patients
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14
Q

Treatment for hypoglycemia:

A

10% dextrose infusion, 50% dextrose push, and/or stop insulin administration

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15
Q

Higher insulin doses increase risk of rebound hypoglycemia – what can you do to avoid this?

A

Use 1-2 hour taper down of the infusion to stop PN

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16
Q

What should you recommend If PN needs to be stopped abruptly?

A
  • infuse dextrose containing solution for 1-2 hours after d/c
  • Obtain fingersticks 30-60 minutes after PN is stopped to check for rebound hypoglycemia
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17
Q

EFAD clinical signs

A
  • scaly dermatitis
  • poor wound healing
  • alopecia
  • thrombocytopenia
  • fatty liver
  • anemia
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18
Q

What triene:tetraene ratio indicates EFAD?

A

Triene:tetraene ratio of > 0.2 indicates EFAD
* Can occur within 1-3 weeks in adults receiving ILE free PN

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19
Q

Adult requirements for linoleic acid are met through:

A

Exogenous sources

Endogenously through lipolysis of adipose tissue
* When dextrose is infused, insulin is secreted and lipolysis is reduced
* So exogenous fat source must be provided

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20
Q

Daily requirements of linolenic and linoleic acids

A
  • Linoleic acid: 1-2% daily energy requirements
  • Linolenic acid: 0.5% of energy
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21
Q

Daily requirements as ILE dosing
Intralipid (soy)

A

250ml 20% soy-based ILE over 8-10 hours 2x/week
500ml 10% soy-based ILE 1x/week

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22
Q

Daily requirements as ILE dosing
SMOF:

A

daily dose of 25.1g (125.7 ml) for a 2000 kcal diet

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23
Q

Soy based ILEs have been associated with:

A
  • Immunosuppressive effects
  • Reticuloendothelial system dysfunction
  • Exaggerated inflammatory response
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24
Q

What has been suggested as a strategy to reduce immunosuppression complications with ILE administration in critically ill patients?

A

Withholding or limit soy-based ILE in critically ill patients for the first week of PN has been suggested as a strategy to reduce immunosuppression complications

2016 ASPEN/SCCM: support this recommendation, but – very low rating of evidence

Based on 1 study (on trauma patients receiving fat-free PN in the first 10 days hospitalization)
>20 years old, not duplicated
Criticisms r/t goals for energy delivery based on nonprotein calories (not total kcal)

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25
Q

Cause of hypertriglyceridemia in PN

A

Result of dextrose overfeeding or rapid administration of ILE (>0.11 gm/kg/hr)

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26
Q

What can hypertriglyceridemia do?

What is an appropriate response with PN administration if pt has high TG?

A
  • May impair immune response
  • alter pulmonary hemodynamics
  • increase risk of pancreatitis
  • Reduce dose and/or lengthening infusion time of ILE can help minimize these effects
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27
Q

ILE should not exceed what amount for a day?

A

ILE should be less than 30% of total energy (or 1 g/kg/day)

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28
Q

ASPEN recommendation for PN, ILE, and hypertriglyceridemia:

A

if TG >400, reduce dose or discontinue ILE

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29
Q

Is ILE considered safe for use in patients with pancreatitis?

A

ILE is considered safe for use in patients with pancreatitis without hypertriglyceridemia

Pancreatitis 2/2 ILE hypertriglyceridemia is rare unless TG >1000

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30
Q

What organ can also impact TG level?

A

Renal impairment can impact TG level

Increased TG in CKD = delayed catabolism of TG-rich lipoproteins

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31
Q

Adverse reaction to ILE

A
  • Rare, but can occur – especially in patients with history of egg allergy
  • Likely 2/2 egg phospholipid that’s used as an emulsifier
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32
Q

Prerenal azotemia:

A

can result from dehydration, excess protein, and/or inadequate energy from non-protein sources (ex: pts with anorexia nervosa)

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33
Q

Why are renal and hepatic patients predisposed to developing azotemia?

A
  • Ability to metabolize and eliminate urea is impaired
  • When urea clearance is impaired, pts may require HD to eliminate urea and allow adequate protein intakes
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34
Q

Why does hyperammonemia rarely occur now with PN administration?

A

Hyperammonemia rarely occurs now that crystalline AA are used in PN

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35
Q

Hyperammonemia has been observed in which patient population on PN?

A

Urea cycle defects (ex: ornithine transcarbamylase deficiency)
* Ornithine transcarbamylase is a zinc enzyme involved in the urea cycle
* Its activity decreases because of zinc deficiency
* Results in reduced hepatic capacity to metabolize ammonia

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36
Q

What would patients on PN potentially benefit from in Prerenal azotemia?

A

pts may benefit from reduction in amount of AA provided

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37
Q

Why are high BCAA, low aromatic AA not recommended in PN for hepatic failure and hepatic encephalopathy?

A

inconsistent results and is not recommended

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38
Q

Protein should NOT be restricted – especially when malnourished - in which patient population?

A

Critical illness & CRRT/HD

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39
Q

Prior to PN start, evaluate:

A
  • vital signs
  • I/Os
  • physical exam
  • CMP, phosphate, magnesium
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40
Q

PN & Warfarin: Why is close monitoring needed?

A

Parenteral MVI (150 mcg) and ILE both contain vitamin K

41
Q

Thiamin deficiency can cause

A

lactic acidosis

42
Q

What nutrients are recommended for first 5-7 days of PN for patients with a history of poor PO intakes?

A

Supplemental thiamin (50-100 mg/day) and folic acid (1 mg/day)

43
Q

What nutrient toxicity is reported in PN patients with renal failure?

A

Vitamin A

44
Q

What is the recommendation regarding fat soluble vitamins in PN/renal pts?

A
  • Reduce frequency of fat-soluble vitamin administration to 2x/week in these patients
  • This decreases amount of water soluble provided → deficiency from losses with HD/inadequate intakes
  • Provide PO B-complex, or parenteral B vitamin supplementation
45
Q

Several vitamins undergo degradation after addition to the PN formulation. Who is this a concern for?

A
  • Not concerning in acute care
  • Batch compounding for home PN patients is a concern
46
Q

To address vitamin/mineral losses in batch compounded home PN:

A

Patients have to add vitamins themselves to PN before administering

Losses likely 2/2 degradation and absorption to plastic matrix of bag

47
Q

Shortages of MVI,
ration use by:

A
  • Reducing the dose by 50%
  • giving 1 dose 3x/week
  • or use oral/enteral as able
48
Q

If IV MVI are no longer available, give the patient:

A

thiamin, ascorbic acid, pyridoxine and folic acid daily

49
Q

cardiomyopathy – reported in long-term PN without what trace element?

A

Selenium

50
Q

Consider reducing which trace elements in patients with hepatobiliary disease?

A

Manganese and copper

  • especially for long term use
  • d/t impaired excretion, to minimize risks of toxicity
51
Q

How long can MTE be held for newly initiated adult patients who are not critically ill and do not have pre-existing deficits?

A

for the first month of PN therapy

52
Q

Why is Iron is not a component of PN?

A

because of compatibility limitations

53
Q

In refeeding syndrome, CHO administration increases demand for intracellular Phos to

A

synthesize ATP resulting in further depletion of phosphorous

54
Q

What happens during refeeding when there are thiamin, magnesium, phosphorous, and potassium deficits?

A

Deficits cause neuromuscular, cardiovascular, and respiratory compromise

55
Q

Why does fluid overload and edema occur in refeeding syndrome?

A

Fluid and sodium from nutrition delivery burdens compromised organs

56
Q

can you start at goal dose protein in a patient at risk for refeeding?

A

Since effect of protein on glycolysis is not as concerning as dextrose, starting at goal dose (1.2-1.5 g/kg/d) is recommended

Recommendations differ

57
Q

Steatosis & PN

A
  • Hepatic fat accumulation
  • More common in adults
  • Modest elevations of aminotransferase concentrations within 2 weeks of PN initiation and usually return to normal (even when PN is continued)
  • Usually related to overfeeding
58
Q

Cholestasis & PN

A
  • Impaired secretion of bile or frank biliary obstruction
  • Primarily occurs in children, but can occur in adults receiving long-term PN
  • Presents as elevated Alk Phos, GGT, and conjugated (direct) bilirubin with or without jaundice
  • D Bili > 2 is prime indicator for cholestasis
59
Q

Cholestasis has been associated with ILE doses

A

> 1g/kg/day in adult patients receiving long-term PN

60
Q

Gallbladder sludge/stones & PN

A
  • Related to lack of enteral stimulation
  • Related to duration of PN therapy (8-10 weeks)
61
Q

Prevalence of hepatobiliary complications

A

Adult PNALD: 25-100%

Risk and severity of liver disease increase as the duration of PN usage lengthens

  • Bacterial and fungal infections
  • Sepsis likely causes liver inflammation because of the release of proinflammatory cytokines
  • Relevant in recurrent central line infections for long-term PN pts
  • Many patients receiving PN have disorders that predispose them to SIBO which is another risk factor for liver disease
  • Small bowel < 50 cm significantly associated with chronic cholestasis
62
Q

Dextrose-based PN can result in EFAD →

A

impaired lipoprotein formation and TG secretion → steatosis

63
Q

What is a balanced PN formulation (r/t fat and CHO)?

A
  • 70-85% nonprotein energy as CHO
  • 15-30% as fat
64
Q

Early AA formulations had a significant amount of _ _ _ contamination

A

Aluminum

65
Q

New AA formulations are crystalline which has

A

reduced aluminum toxicity rates

66
Q

Phytosterols in ILE

A

Are inefficiently metabolized to bile acids by the liver
* They are hepatotoxic
* May impair bile flow and cause biliary sludge and stones

67
Q

Carnitine supplementation:

A

No set guidelines for supplementation at this time

68
Q

Carnitine is Important in

A

Fat metabolism
Not routinely used in PN

69
Q

Primary carnitine deficiency has been associated with the development of

A

steatosis

70
Q

What is choline required for?

A

Lipid transport and metabolism

71
Q

Is carnitine a part of PN formulations?

A

Carnitine is NOT a part of PN formulations because It is assumed endogenous synthesis is possible from methionine contained in the crystalline amino acid solution

72
Q

Conversion of methionine to choline may be less efficient when given

A

Parenterally
(vs orally)

73
Q

Why is PO/EN preferred over PN during PN complications?

A

Optimize when possible because it promotes enterohepatic circulation of bile acids

74
Q

SBS patients on PN should be encouraged to:

A
  • Maximize oral intake because some of their intake will be absorbed
  • Fluid requirements generally stay the same
75
Q

Is EN feasible in Chronic intestinal pseudo-obstruction dependent on PN and gastric decompression?

A
  • May tolerate jejunal feeds at slow rate
  • May require promotility agents
  • Multiple trials may be required before achieving tolerance
76
Q

Cyclic PN

A

Shown to reduce serum liver enzyme and D.bili concentrations when compared to continuous

77
Q

Ursodiol & PN

A

Form of bile acid widely used to treat chronic cholestatic liver diseases
* Shown to improve biochemical markers of cholestasis
* When administered, it’s thought to become the predominant biliary bile acid and displaces potentially hepatotoxic bile salts
* Only available in oral form

78
Q

CMS criteria to define PN failure –

A

development of impending or overt liver failure

79
Q

Osteoporosis:

A

low bone mass, compromised bone strength, deterioration of bone tissue

80
Q

Osteomalacia:

A

softening and bending of the bones,
usually caused by vitamin D deficiency

81
Q

Prevalence of Metabolic Bone Disease

A
  • 41% in patients on TPN for 6 months
  • 67% in those with intestinal failure
  • Unclear whether PN itself contributes to accelerated bone loss
  • Many additional risk factors outside of PN
82
Q

Calcium Function

A

Maintains bone integrity by decreasing bone turnover and slowing bone loss

83
Q

The most important contributor to metabolic bone disease is

A

a negative calcium balance

84
Q

Hypocalcemia occurs as a result of

A

decreased calcium intake and/or increased calcium urinary excretion.

85
Q

Factors that cause hypercalciuria include: excessive calcium and inadequate phosphorus supplementation, excessive protein in PN solutions, cyclic PN infusions, and chronic metabolic acidosis.

A
86
Q

ASPEN rx for calcium in PN:

A

10-15 mEq/d calcium gluconate in PN

Higher Ca doses in PN are offset by higher urinary calcium losses

87
Q

An inadequate phosphorous dose - impact on calcium

A

increase urinary calcium excretion

88
Q

ASPEN rx for phos in PN:

A

20-40 mmol/d

Phos seems to enhance calcium reabsorption by renal tubules → positive calcium balance

89
Q

What is associated with hypercalciuria and metabolic bone disease?

A

Chronic metabolic acidosis

Correction with acetate can reduce urinary calcium excretion

90
Q

calcium

High protein doses (2g/kg/d vs 1g/kg/d) in PN have been associated with

A

urinary calcium excretion in adults

Recommend: reduce protein to maintenance dose whenever possible

91
Q

Cyclic PN & calcium

A

Cyclic PN infusion results in higher urinary calcium losses when compared to continuous

92
Q

Excessive doses of Vitamin D

A

suppress PTH secretion and directly promote bone resorption

93
Q

Aluminum contamination can lead to

A

bone disease

94
Q

FDA requires labeling of aluminum content and disclose on the labels. Large volume parenteral products (amino acid, dextrose, ILE solutions) are required to contain:

A

no more than 25 mcg aluminum per liter

95
Q

FDA does not limit aluminum content in small-volume PN products (electrolyte salts) and pharmacy bulk packages (PN MVI and MTE). Manufacturers are required to

A

state the max aluminum level at expiry in the product labeling

96
Q

Hypocalcemia is a prominent manifestation of what deficiency?

A

magnesium deficiency

97
Q

Hypomagnesemia can lead to:

A

Hypophosphatemia because of increased phosphorous excretion

98
Q

What Deficiency impairs bone formation and can cause osteoporosis?

A

Copper deficiency

[Mine] core curric - 2016 (22 decks)

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