Ch 17: Complications of Parenteral Nutrition Flashcards
Serum triglycerides provide a reasonable estimate of
ASPEN self assessment - PN
body lipid clearance
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
- within 2 weeks
- elevated AST, ALT
- confirmed by triene: tetraene ratio.
Recommended dosage for all types of ILE are _ _ _ g/kg/day.
Lipid dosing should not to exceed _ _ _ g/kg/day
ASPEN self assessment - PN
1-2g/kg/day,
not to exceed 2.5g/kg/day
What deficiency exacerbates lipid abnormalities?
Existing evidence has not confirmed that supplementation corrects _ _ _
ASPEN self assessment - PN
L-carnitine
hypertriglyceridemia
Most common complication associated with PN
Hyperglycemia
Stress associated causes of hyperglycemia
- insulin resistance
- increased gluconeogenesis and glycogenolysis
- suppressed insulin secretion
Excess CHO administration →
- hyperglycemia
- hepatic steatosis
- increase CO2 production
Target BG levels per ASPEN and SCCM
- ASPEN: 140-180 mg/dL in adult hospitalized patients receiving nutrition support
- SCCM: 150-180 mg/dL for ICU populations
Insulin therapy in PN
- 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
How much of the total amount of SSI required over 24 hours may be added to the next day PN?
Two-thirds
Hyperglycemia is associated with worsened clinical outcomes:
- increased risk of infection
- poor wound healing
- inability to gain weight
Do not exceed a GIR of _ _ _ from CHO in acutely ill patients
4-5 mg/kg/d
(20-25 kcal)
What nutrient deficiency can cause hyperglycemia?
- Rarely, hyperglycemia may be related to chromium deficiency
- Insulin is less effective in these patients
Treatment for hypoglycemia:
10% dextrose infusion, 50% dextrose push, and/or stop insulin administration
Higher insulin doses increase risk of rebound hypoglycemia – what can you do to avoid this?
Use 1-2 hour taper down of the infusion to stop PN
What should you recommend If PN needs to be stopped abruptly?
- 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
EFAD clinical signs
- scaly dermatitis
- poor wound healing
- alopecia
- thrombocytopenia
- fatty liver
- anemia
What triene:tetraene ratio indicates EFAD?
Triene:tetraene ratio of > 0.2 indicates EFAD
* Can occur within 1-3 weeks in adults receiving ILE free PN
Adult requirements for linoleic acid are met through:
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
Daily requirements of linolenic and linoleic acids
- Linoleic acid: 1-2% daily energy requirements
- Linolenic acid: 0.5% of energy
Daily requirements as ILE dosing
Intralipid (soy)
250ml 20% soy-based ILE over 8-10 hours 2x/week
500ml 10% soy-based ILE 1x/week
Daily requirements as ILE dosing
SMOF:
daily dose of 25.1g (125.7 ml) for a 2000 kcal diet
Soy based ILEs have been associated with:
- Immunosuppressive effects
- Reticuloendothelial system dysfunction
- Exaggerated inflammatory response
What has been suggested as a strategy to reduce immunosuppression complications with ILE administration in critically ill patients?
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)
Cause of hypertriglyceridemia in PN
Result of dextrose overfeeding or rapid administration of ILE (>0.11 gm/kg/hr)
What can hypertriglyceridemia do?
What is an appropriate response with PN administration if pt has high TG?
- 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
ILE should not exceed what amount for a day?
ILE should be less than 30% of total energy (or 1 g/kg/day)
ASPEN recommendation for PN, ILE, and hypertriglyceridemia:
if TG >400, reduce dose or discontinue ILE
Is ILE considered safe for use in patients with pancreatitis?
ILE is considered safe for use in patients with pancreatitis without hypertriglyceridemia
Pancreatitis 2/2 ILE hypertriglyceridemia is rare unless TG >1000
What organ can also impact TG level?
Renal impairment can impact TG level
Increased TG in CKD = delayed catabolism of TG-rich lipoproteins
Adverse reaction to ILE
- Rare, but can occur – especially in patients with history of egg allergy
- Likely 2/2 egg phospholipid that’s used as an emulsifier
Prerenal azotemia:
can result from dehydration, excess protein, and/or inadequate energy from non-protein sources (ex: pts with anorexia nervosa)
Why are renal and hepatic patients predisposed to developing azotemia?
- 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
Why does hyperammonemia rarely occur now with PN administration?
Hyperammonemia rarely occurs now that crystalline AA are used in PN
Hyperammonemia has been observed in which patient population on PN?
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
What would patients on PN potentially benefit from in Prerenal azotemia?
pts may benefit from reduction in amount of AA provided
Why are high BCAA, low aromatic AA not recommended in PN for hepatic failure and hepatic encephalopathy?
inconsistent results and is not recommended
Protein should NOT be restricted – especially when malnourished - in which patient population?
Critical illness & CRRT/HD
Prior to PN start, evaluate:
- vital signs
- I/Os
- physical exam
- CMP, phosphate, magnesium
PN & Warfarin: Why is close monitoring needed?
Parenteral MVI (150 mcg) and ILE both contain vitamin K
Thiamin deficiency can cause
lactic acidosis
What nutrients are recommended for first 5-7 days of PN for patients with a history of poor PO intakes?
Supplemental thiamin (50-100 mg/day) and folic acid (1 mg/day)
What nutrient toxicity is reported in PN patients with renal failure?
Vitamin A
What is the recommendation regarding fat soluble vitamins in PN/renal pts?
- 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
Several vitamins undergo degradation after addition to the PN formulation. Who is this a concern for?
- Not concerning in acute care
- Batch compounding for home PN patients is a concern
To address vitamin/mineral losses in batch compounded home PN:
Patients have to add vitamins themselves to PN before administering
Losses likely 2/2 degradation and absorption to plastic matrix of bag
Shortages of MVI,
ration use by:
- Reducing the dose by 50%
- giving 1 dose 3x/week
- or use oral/enteral as able
If IV MVI are no longer available, give the patient:
thiamin, ascorbic acid, pyridoxine and folic acid daily
cardiomyopathy – reported in long-term PN without what trace element?
Selenium
Consider reducing which trace elements in patients with hepatobiliary disease?
Manganese and copper
- especially for long term use
- d/t impaired excretion, to minimize risks of toxicity
How long can MTE be held for newly initiated adult patients who are not critically ill and do not have pre-existing deficits?
for the first month of PN therapy
Why is Iron is not a component of PN?
because of compatibility limitations
In refeeding syndrome, CHO administration increases demand for intracellular Phos to
synthesize ATP resulting in further depletion of phosphorous
What happens during refeeding when there are thiamin, magnesium, phosphorous, and potassium deficits?
Deficits cause neuromuscular, cardiovascular, and respiratory compromise
Why does fluid overload and edema occur in refeeding syndrome?
Fluid and sodium from nutrition delivery burdens compromised organs
can you start at goal dose protein in a patient at risk for refeeding?
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
Steatosis & PN
- 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
Cholestasis & PN
- 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
Cholestasis has been associated with ILE doses
> 1g/kg/day in adult patients receiving long-term PN
Gallbladder sludge/stones & PN
- Related to lack of enteral stimulation
- Related to duration of PN therapy (8-10 weeks)
Prevalence of hepatobiliary complications
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
Dextrose-based PN can result in EFAD →
impaired lipoprotein formation and TG secretion → steatosis
What is a balanced PN formulation (r/t fat and CHO)?
- 70-85% nonprotein energy as CHO
- 15-30% as fat
Early AA formulations had a significant amount of _ _ _ contamination
Aluminum
New AA formulations are crystalline which has
reduced aluminum toxicity rates
Phytosterols in ILE
Are inefficiently metabolized to bile acids by the liver
* They are hepatotoxic
* May impair bile flow and cause biliary sludge and stones
Carnitine supplementation:
No set guidelines for supplementation at this time
Carnitine is Important in
Fat metabolism
Not routinely used in PN
Primary carnitine deficiency has been associated with the development of
steatosis
What is choline required for?
Lipid transport and metabolism
Is carnitine a part of PN formulations?
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
Conversion of methionine to choline may be less efficient when given
Parenterally
(vs orally)
Why is PO/EN preferred over PN during PN complications?
Optimize when possible because it promotes enterohepatic circulation of bile acids
SBS patients on PN should be encouraged to:
- Maximize oral intake because some of their intake will be absorbed
- Fluid requirements generally stay the same
Is EN feasible in Chronic intestinal pseudo-obstruction dependent on PN and gastric decompression?
- May tolerate jejunal feeds at slow rate
- May require promotility agents
- Multiple trials may be required before achieving tolerance
Cyclic PN
Shown to reduce serum liver enzyme and D.bili concentrations when compared to continuous
Ursodiol & PN
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
CMS criteria to define PN failure –
development of impending or overt liver failure
Osteoporosis:
low bone mass, compromised bone strength, deterioration of bone tissue
Osteomalacia:
softening and bending of the bones,
usually caused by vitamin D deficiency
Prevalence of Metabolic Bone Disease
- 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
Calcium Function
Maintains bone integrity by decreasing bone turnover and slowing bone loss
The most important contributor to metabolic bone disease is
a negative calcium balance
Hypocalcemia occurs as a result of
decreased calcium intake and/or increased calcium urinary excretion.
Factors that cause hypercalciuria include: excessive calcium and inadequate phosphorus supplementation, excessive protein in PN solutions, cyclic PN infusions, and chronic metabolic acidosis.
ASPEN rx for calcium in PN:
10-15 mEq/d calcium gluconate in PN
Higher Ca doses in PN are offset by higher urinary calcium losses
An inadequate phosphorous dose - impact on calcium
increase urinary calcium excretion
ASPEN rx for phos in PN:
20-40 mmol/d
Phos seems to enhance calcium reabsorption by renal tubules → positive calcium balance
What is associated with hypercalciuria and metabolic bone disease?
Chronic metabolic acidosis
Correction with acetate can reduce urinary calcium excretion
calcium
High protein doses (2g/kg/d vs 1g/kg/d) in PN have been associated with
urinary calcium excretion in adults
Recommend: reduce protein to maintenance dose whenever possible
Cyclic PN & calcium
Cyclic PN infusion results in higher urinary calcium losses when compared to continuous
Excessive doses of Vitamin D
suppress PTH secretion and directly promote bone resorption
Aluminum contamination can lead to
bone disease
FDA requires labeling of aluminum content and disclose on the labels. Large volume parenteral products (amino acid, dextrose, ILE solutions) are required to contain:
no more than 25 mcg aluminum per liter
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
state the max aluminum level at expiry in the product labeling
Hypocalcemia is a prominent manifestation of what deficiency?
magnesium deficiency
Hypomagnesemia can lead to:
Hypophosphatemia because of increased phosphorous excretion
What Deficiency impairs bone formation and can cause osteoporosis?
Copper deficiency
