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ASPEN Adult Nutrition Support Core Curriculum for CNSC Exam > Complications of Parenteral Nutrition > Flashcards

Complications of Parenteral Nutrition Flashcards

1
Q

What is the most common metabolic complication associated with PN?

A

Hyperglycemia

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2
Q

Cholestasis has been associated with ILE doses greater than __ gm/kg/day in adult patients receiving long term PN

A

1 gm/kg/day

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3
Q

ASPEN recommended phosphorus dose for PN formulation?

A

20-40 mmol/day

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4
Q

What is calcium supplementation in PN limited by?

A

Limited by calcium’s physical compatibility with phosphorus

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5
Q

How can excessive vitamin D be detrimental to the bone?

A

Excessive vitamin D can suppress parathyroid hormone and promote bone resorption

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6
Q

How does stress-associated hyperglycemia develop?

A

As a result of insulin resistance, increased gluconeogenesis, and suppressed insulin secretion

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7
Q

What is the ASPEN recommended target BG concentration in adult hospitalized patients?

A

140-180 mg/dL

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8
Q

What conditions has excessive carbohydrate administration been associated with?

A

Hyperglycemia, hepatic steatosis, and increased carbon dioxide production

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9
Q

In acutely ill patients, carbohydrate administration should not exceed a rate of:

A

4-5 mg/kg/min or 20-25 kcal/kg/day

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10
Q

When would the delivery of ~100 gm dextrose be warranted?

A

If the patient has a low BMI or poor glucose control

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11
Q

How often should capillary blood glucose concentrations be monitored in patients receiving short-acting subcutaneous insulin?

A

Every 6-8 hours

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12
Q

What is a common initial insulin regimen in PN?

A

0.05 to 0.1 units per gram of dextrose
0.15 to 0.2 units per gram of dextrose if patient is already hyperglycemic

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13
Q

What kind of insulin should be added to the PN formulation?

A

Regular insulin

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14
Q

What clinical outcomes is hyperglycemia associated with?

A

Increased risk of infection
Poor wound healing
Inability to gain weight

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15
Q

How can PN-associated hypoglycemia occur?

A

Excess insulin administration via the PN solution, IV infusion, or subcutaneous injection

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16
Q

What are treatment methods for PN-associated hypoglycemia?

A

Initiation of a 10% dextrose infusion, administration of an ampule of 50% dextrose, and/or stopping any source of insulin administration. Can also consider oral carbohydrate (glucose gel or chewable tablets) in mild hypoglycemia in patients who can tolerate it

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17
Q

What has been associated with rebound hypoglycemia?

A

Abrupt discontinuation of PN

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18
Q

How can the risk of rebound hypoglycemia be reduced?

A

1- to 2-hour taper down of the infusion, or half the infusion rate

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19
Q

What should be done if a PN solution must be discontinued quickly?

A

A dextrose-containing fluid should be infused for 1 to 2 hours following PN discontinuation to avoid a possible rebound hypoglycemia

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20
Q

ILE-free PN may result in what deficiency?

A

Essential fatty acid deficiency (EFAD)

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21
Q

What are clinical manifestations of EFAD?

A

Scaly dermatitis
Alopecia
Hepatomegaly
Thrombocytopenia
Fatty liver
Anemia

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22
Q

After what length of time receiving an ILE-free PN can EFAD occur?

A

Within 1-3 weeks in adults receiving ILE-free PN

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23
Q

Adult requirements for linoleic acid are met through exogenous sources or endogenously through the lipolysis of adipose tissue, but what can happen when hypertonic dextrose is infused?

A

Insulin is secreted and lipolysis is reduced, necessitating an exogenous source of fat provision

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24
Q

To prevent EFAD, what percent of daily energy requirements should be derived from linoleic acid and linolenic acid?

A

1-2% from linoleic acid
0.5% from linolenic acid

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25
Q

What is the infusion goal of 10% and 20% soy-based ILE administration to prevent EFAD?

A

500 ml of 10% soy-based ILE administered over 8-10 hours twice a week OR
250 ml of 20% soy-based ILE administered over 8-10 hours twice a week OR
500 ml of a 20% soy-based ILE given once a week

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26
Q

What needs to be considered (regarding preventing EFAD) when using an alternative oil-based ILE (such as those containing MCTs, olive oil, fish oil)?

A

A greater amount of ILE is required to meet essential fatty acid requirements because these non-soy based products contain lower quantities of linoleic and linolenic acid

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27
Q

How has linoleic acid (aka omega-6) been postulated to suppress the immune response?

A

By activating the arachidonic pathway

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28
Q

How is it suggested that certain long-chain fatty acids may impair immune function?

A

By interfering with phagocytosis and chemotaxis and may increase the patient’s risk of infection

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29
Q

What has been suggested as a strategy to reduce immunosuppression complications in critically ill patients receiving PN?

A

Withholding or limiting soy-based ILE for the first week of PN - recommendation based primarily on research from only 1 study

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30
Q

When can hypertriglyceridemia occur with PN?

A

With dextrose overfeeding or with rapid administration rates of ILE (>0.11 gm/kg/hour)

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31
Q

What complications may result from hyperlipidemia?

A

May impair immune response, alter pulmonary hemodynamics, increase risk of pancreatitis

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32
Q

What amount should ILE intake be restricted to?

A

<30% of total energy, or 1gm/kg/day

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33
Q

What are the ASPEN recommendations regarding serum triglyceride levels and the appropriate response?

A

Serum TG >400 mg/dL should be avoided when infusing ILE, and the ILE dose should be reduced or discontinued if this level of hypertriglyceridemia occurs

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34
Q

Why should the dose of ILE be reduced or discontinued in the mechanically ventilated patient receiving Propofol?

A

Because Propofol is supplied as a 10% ILE

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35
Q

Is ILE considered safe for use in pancreatitis without hypertriglyceridemia?

A

Yes

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36
Q

What condition is rare unless serum TG levels exceed 1000 mg/dL?

A

Pancreatitis due to ILE-induced hyperlipidemia

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37
Q

What happens when protein administration is excessive?

A

The metabolic demand of disposing of the byproducts of protein metabolism increases

38
Q

Why are patients with hepatic or renal disease prone to developing azotemia?

A

Because their ability to metabolize and eliminate urea is impaired

39
Q

What can cause prerenal azotemia?

A

Dehydration, excess protein, and/or inadequate energy from nonprotein sources

40
Q

Should protein be restricted in critically ill patients with AKI?

A

Not if they are receiving CRRT or HD, especially in the setting of malnutrition

41
Q

If a patient has excessive fluid losses, should fluid and electrolyte replacement be added to the PN formulation or provided separately?

A

Separately

42
Q

What parameters should be monitored, and with what frequency, to help identify and prevent metabolic complications in a patient initiating PN?

A

Before PN is initiated, should evaluate patient’s vital signs, I/O, and physical exam data to determine their fluid status. Complete metabolic panel including phos and magnesium. PN may be administered slowly and titrated to goal over a period of days to prevent hyperglycemia. BG levels monitored at least every 6 hours until patient is euglycemic

43
Q

What situations may complicate provision of adequate vitamin intake in the PN?

A

Conditions that increase requirements, such as sepsis, trauma, or recovery following surgery

44
Q

Why can identifying vitamin deficiency or toxicity be difficult?

A

Serum vitamin concentrations do not always directly correlate with body stores and clinical symptoms are often nonspecific

45
Q

Why do patients receiving both PN and warfarin therapy require close monitoring?

A

Because the vitamin K (150 mcg) included in the 13-vitamin preparation interacts with warfarin and can result in therapeutic failure

46
Q

Patients with a history of prolonged poor dietary intake or alcohol abuse are at risk for what deficiency?

A

Thiamin

47
Q

What amount of additional supplemental thiamin and folic acid is recommended (beyond what is provided in the PN multivitamin preparation) for the initial 5-7 days of PN therapy for patients with a history of prolonged poor dietary intake?

A

50-100 mg thiamin
1 mg folic acid

48
Q

In what population has vitamin A toxicity been reported in those patients receiving PN?

A

Renal failure

49
Q

What needs to be considered regarding vitamin addition to PN solution for home infusion?

A

PN is compounded in a batch fashion for the home setting. Several vitamins are known to undergo substantial degradation after addition to the PN formula. In the home setting, the patient or caregiver must perform the task of adding vitamins to the PN formulation prior to administration

50
Q

ASPEN advice to help clinicians cope with parenteral multivitamin product shortages:

A

Reserve a supply of IV multivitamins for those patients receiving solely PN
Use oral or enteral MVI whenever possible
Do not stockpile parenteral MVI
Do not use pediatric IV multivitamin for adults
Ration use by reducing the dose by 50% or by giving 1 dose 3 times/week when all options to obtain IV MVI have been exhausted
Administer individual thiamin, ascorbic acid, pyridoxine, and folic acid daily if IV MVI are no longer available

51
Q

Under what circumstances could trace element deficiency occur (also name specific situations)?

A

When intake is insufficient or utilization or excretion is increased over a prolonged period. Patient with high intestinal output may become zinc deficient. Cardiomyopathy caused by selenium deficiency has been reported in patients receiving long-term PN without selenium supplementation

52
Q

True or False: Available parenteral multi-trace element preparations may be lacking in actual requirements in patients receiving PN

A

False. May exceed actual requirements

53
Q

Why should clinicians consider reducing manganese and copper dosing in patients with hepatobiliary disease?

A

The hepatobiliary disease impairs excretion

54
Q

What are the ASPEN suggestions when facing a parenteral multi-trace element shortage?

A

Reducing doses in half
Limiting the frequency of administration to 3x/week
Using oral/enteral route when feasible
Withholding multi-trace elements for the first month of PN therapy in newly initiated adult patients who are not critically ill and do not have preexisting deficits

55
Q

What is the time frame after initiation of nutrition support when refeeding syndrome is a risk?

A

During the first 2-5 days after the start of nutrition support

56
Q

In periods of prolonged starvation, how does the body adapt?

A

By deriving energy from fat (ketone production), reducing energy expenditure, decreasing insulin secretion, and utilizing intracellular minerals and electrolytes

57
Q

How can complications of refeeding syndrome be minimized when providing PN to a nutritionally depleted patient?
Scenario: Patient w/ h/o gastric cancer s/p partial gastrectomy and small bowel resection. NG output 1250 ml/day w/ SBO. BMI 20, UBW 75 kg, currently 66 kg. Shows evidence of moderate muscle and fat wasting with slight edema

A

Start nutrition slowly by providing half of the goal energy requirements (~15 kcal/kg/day) on the first day of PN. First bag should contain about 1000 kcal. Start at goal protein dose (1.2-1.5 g/kg/day). Dextrose and fat should comprise the rest of the formulation (dextrose not to exceed 200 gm/day). Slowly advance to goal over the next 2-5 days while monitoring electrolytes daily (Na, K+, Phos, Mg). Administer vitamins and trace elements daily

58
Q

Aside from refeeding syndrome, what other conditions may cause refeeding hypophosphatemia?

A

Cellular phosphate redistribution, poor phosphate intake, or renal tubular phosphate loss

59
Q

What are the 3 types of hepatobiliary disorders associated with PN therapy?

A

Steatosis (hepatic fat accumulation), cholestasis, and gallbladder sludge/stones

60
Q

The term PN-induced liver disease has been replaced with which two interchangeable terms?

A

PN-associated liver disease (PNALD) and intestinal failure-associated liver disease

61
Q

How does steatosis typically present?

A

Modest elevations of serum aminotransferase (aka transaminase) concentrations that occur within 2 weeks of PN therapy, and concentrations may return to normal even when PN is continued. Most patients are asymptomatic

62
Q

What does steatosis seem to be a complication of during PN therapy?

A

Complication of overfeeding. Has probably decreased in prevalence over the years as estimates of PN energy requirements have been lowered

63
Q

What may steatosis progress to?

A

May progress to fibrosis or cirrhosis in patients receiving long-term PN

64
Q

What is PN-associated cholestasis (PNAC)?

A

A condition of impaired secretion of bile or frank biliary obstruction that occurs predominantly in children, but may occur in adult patients receiving long-term PN

65
Q

How does PNAC typically present?

A

Elevated alkaline phosphatase, GGT, and direct bilirubin with or without jaundice.

66
Q

What is the prime indicator for cholestasis?

A

A direct bilirubin >2 mg/dL

67
Q

Why is PNAC considered a serious complication?

A

It may progress to cirrhosis and liver failure

68
Q

What may gallbladder stasis during PN therapy progress to?

A

The development of gallstones or gallbladder sludge with subsequent cholecystitis

69
Q

Rather than being related to PN infusion itself, what is gallbladder stasis during PN therapy more related to?

A

The lack of enteral stimulation which results in decreased cholecystokinin release and impaired bile flow and gallbladder contractility. Duration of PN therapy seems to correlate with the development of biliary sludge

70
Q

What is acalculous cholecystitis?

A

Biliary sludge progressing to acute cholecystitis in the absence of gallstones

71
Q

The risk for and severity of liver disease increases or decreases as the duration of PN usage lengthens?

A

Increases

72
Q

What are risk factors for PNALD that are unrelated to the PN therapy itself?

A

Bacterial and fungal infections (associated with cholestasis)
Sepsis (likely causes liver inflammation due to release of proinflammatory cytokines) and recurrent central line-associated bloodstream infections
SIBO
Massive intestinal resection
Small bowel remnant <50 cm in length

73
Q

What is the development of steatosis during PN administration primarily related to?

A

Excessive energy intake, promotes hepatic fat deposition by stimulating insulin release, which in turn promotes lipogenesis and inhibits fatty acid oxidation

74
Q

What complications may arise from dextrose-based PN that contains little or no fat?

A

Development of steatosis. Excess carbs deposit in the liver as fat. Dextrose-based PN may result in EFAD which may lead to impaired lipoprotein formation and triglyceride secretion, resulting in steatosis

75
Q

A balanced PN formulation should provide __ to __% of nonprotein energy as carbohydrate and __ to __% as fat

A

70-85% of nonprotein energy as carbohydrate
15-30% as fat

76
Q

The carbohydrate content of PN should not exceed __ gm/kg/day in adults

A

7 gm/kg

77
Q

High levels of what trace element exposure may lead to the development of cholestasis?

A

Aluminum

78
Q

How might phytosterols contribute to biliary sludge and stones?

A

They are inefficiently metabolized to bile acids by the liver and may impair bile flow

79
Q

High omega-6 fatty acid content of soybean oil-based ILEs may contribute to what kind of complications?

A

May potentially initiate or worsen inflammatory states and can have immunosuppressive effects

80
Q

What has shown promising effects in reversing PNALD in pediatric patients?

A

Using fish oil-based ILE, primarily composed of omega-3 fatty acids and containing no phytosterols when used in place of a soybean oil-based ILE

81
Q

Chronic cholestasis and severe PNALD were strongly associated with ILE intake greater than __ gm/kg/day in patients receiving long-term PN

A

> 1 gm/kg

82
Q

What has carnitine supplementation to PN been shown to accomplish?

A

Helps mobilize hepatic fat stores and prevent steatosis in neonates receiving PN

83
Q

Why is choline not a component of PN formulations?

A

It is assumed that endogenous synthesis is possible from methionine contained in the crystalline amino acid solution. Also an injectable choline preparation is not commercially available

84
Q

List PN modification strategies to manage PN associated liver complications

A

Decreasing dextrose
Decreasing ILE (<1 gm/kg)
Providing a balance of dextrose and ILE
Cyclic PN infusion

85
Q

List ways to prevent/treat bacterial overgrowth that may contribute to PN associated liver complications

A

Use enteral antibiotics, such as metronidazole, neomycin, doxycycline, ciprofloxacin, or rifaximin
In CIPO patients, consider agents to enhance motility such as metoclopramide or erythromycin

86
Q

List strategies to manage PN associated liver complications

A

Rule out non-PN etiologies for liver problems such as hepatotoxic medications, herbal supplements, biliary obstruction, hepatitis, sepsis
Consider PN modifications
Maximize enteral intake
Prevent/treat bacterial overgrowth
Pharmacotherapy
Consider intestinal transplantation for patients with PN failure

87
Q

How can a PN formulation be modified to minimize and manage the development of cholestasis in an adult patient requiring long-term PN?

A

Could reduce the frequency of ILE from daily to twice weekly and increase dextrose proportionally to account for decrease in energy from lipid
Trial of stopping ILE for 1-2 weeks
Shorten the infusion cycle
Avoid overfeeding
Efforts to minimize the risk of infection

88
Q

Why should oral and enteral nutrition be optimized whenever feasible in the long-term PN patient?

A

Even small amounts of dietary or enteral intake may promote enterohepatic circulation of bile acids

89
Q

How may cyclic PN reduce the risk of PNALD, especially in patients who depend on long-term PN?

A

By reducing liver enzyme and direct bilirubin concentrations when compared with continuous PN infusion

90
Q

Why are patients receiving PN at risk for negative calcium balance?

A

Because of limited intake and increased urinary calcium loss

ASPEN Adult Nutrition Support Core Curriculum for CNSC Exam (19 decks)

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