Lipid Dosing Types of Formulas & Calculations

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Last updated 10:05 PM on 7/31/26
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34 Terms

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name of 4 oil emulsion

SMOFlipid

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<p>SMOFlipid components and function</p>

SMOFlipid components and function

  • S = Soybean oil (30%)

  • M = Medium-chain triglycerides (MCTs) (30%)

  • O = Olive oil (25%)

  • F = Fish oil (15%)

  • 30% soybean oil

    • Provides essential fatty acids (linoleic acid, α-linolenic acid)

  • 30% medium-chain triglycerides (MCTs)

    • Rapidly oxidized for energy

    • Less likely to accumulate

  • 25% olive oil

    • Rich in monounsaturated fats (oleic acid)

    • Relatively neutral inflammatory profile

  • 15% fish oil

    • EPA

    • DHA

    • Anti-inflammatory effects

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1 oil emulsions

Intralipid and Omegaven

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SMOFlipid omega-3 content

Contains EPA & DHA
Contains 15% omega-3 fatty acids from fish oil, providing essential fatty acids that support various physiological processes.

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does intralipid have omega-3s

No, intralipid does not contain omega-3 fatty acids. It's primarily composed of soybean oil and lacks the specific omega-3 supplements found in products like Omegaven.

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does intralipid have MCTs

no

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does SMOFlipid have MCTs

yes

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which has higher phytosterol content intralipid or smoflipid?

intralipid

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which has higher Vitamin E content intralipid or SMOFlipid?

SMOFlipid

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which has higher pro-inflammatory potential intralipid or SMOFlipid?

Intralipid has a higher pro-inflammatory potential compared to SMOFlipid. High omega-6 content in intralipid leads to increased production of arachidonic acid-derived eicosanoids, which tend to promote inflammation. Lower omega-6 plus fish oil in SMOFlipid shifts eicosanoid production toward a less inflammatory profile.

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which is higher in omega-6 content intralipid or SMOFlipid?

intralipid

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<p>intralipid content and functions</p>

intralipid content and functions

  • 100% soybean oil

  • Rich in:

    • Linoleic acid (omega-6)

    • Some α-linolenic acid (omega-3 precursor)

  • Does not provide meaningful amounts of EPA or DHA.

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standard lipid concentration for intralipid and smoflipid for calculations

20%

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volume relationship for calculations for intralipid or SMOFlipid

5 mL/g lipid

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energy density in kcal/mL for intralipid/SMOFlipid

2 kcal/mL

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energy density in kcal/g for intralipid/SMOFlipid

10 kcal/g

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omegaven lipid concentration

10%

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omegaven volume relationship mL/g lipid

10 mL/g lipid

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omegaven kcal/mL

1.1 kcal/mL

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omegaven in kcal/g

11 kcal/g

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MCT oil kcal/mL

7.7 kcal/mL

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lipid in g/d formula

lipid in g/d = dose in g/kg/d x weight in kg

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lipid in mL/d formula

lipid in mL/d = lipid g/d x mL/g

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lipid kcal/d

lipid kcal/d = lipid mL/d x kcal/mL

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lipid infusion rate

(lipid mL/d)/ infusion hours

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A 20% lipid emulsion means how many grams lipid per mL

20 g lipid per 100 mL

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A 10% lipid emulsion means how many grams lipid per mL

10 g lipid per 100 mL

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what % of total kcal should be avoided in lipid dosing and why?

60% of total kcal due to risk of ketosis

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what is the maximum infusion rate and why should this cap be followed?

Do not exceed infusion rate >0.15 gm/kg/hr. To avoid ketosis

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why does ketosis happen secondary to excessive lipid administration

  • triglycerides are hydrolyzed

  • Fatty acids undergo β-oxidation

  • The TCA cycle becomes limited

    • For acetyl-CoA to enter the TCA cycle, it must combine with oxaloacetate.

      Acetyl-CoA + Oxaloacetate → Citrate

      However, if oxaloacetate is relatively unavailable, acetyl-CoA accumulates.

      This occurs when:

      • Carbohydrate intake is inadequate

      • Insulin levels are low

      • Gluconeogenesis consumes oxaloacetate

      • The liver receives an excessive fatty acid load relative to its oxidative capacity

  • Excess acetyl-CoA is diverted to ketogenesis

    • When acetyl-CoA accumulates:

      2 Acetyl-CoA

      Acetoacetyl-CoA

      HMG-CoA

      Acetoacetate

      β-hydroxybutyrate + acetone

      These are the ketone bodies.

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Does excessive lipid alone cause ketosis?

Usually no, especially in patients receiving adequate dextrose.

In PN, sufficient dextrose stimulates insulin, which:

  • suppresses lipolysis,

  • promotes carbohydrate oxidation,

  • maintains oxaloacetate availability, and

  • reduces hepatic ketogenesis.

Therefore, excessive lipid administration by itself does not commonly produce clinically significant ketosis if carbohydrate provision is adequate.

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When can lipid administration contribute to ketosis?

It is more likely when excessive lipid administration occurs along with:

  • inadequate dextrose intake,

  • prolonged fasting,

  • insulin deficiency (e.g., diabetes),

  • severe illness or stress with increased counter-regulatory hormones,

  • inborn errors of carbohydrate metabolism.

In these settings, the liver receives a large fatty acid supply while carbohydrate oxidation is insufficient, favoring ketone production.

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<p>Omegaven content</p>

Omegaven content

highly purified fish oil triglycerides, rich in omega-3s EPA & DHA, added in tocopherol

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Omegaven indication

  • consider if SBS or IF and PN expected > 4 weeks

  • PNAC in absence of other etiologies for cholestasis

  • cautionary use for transient cholestasis

  • not indicated for PNAC prevention