The Complexity of Prescribing Intravenous Lipid Emulsions
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article
Data de publicação
2015
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KARGER
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INTRAVENOUS LIPID EMULSIONS, v.112, p.150-162, 2015
Resumo
Intravenous lipid emulsions (LEs) are relevant for patients receiving parenteral nutrition because they prevent the depletion of essential fatty acids (FAs) and, as a highly dense energy source, enable the reduction of glucose provision, thereby decreasing the risks of hyperglycemia and hepatic impairment. The prescription of LEs is complex, due mainly to their distinct FA components, which may alter the immune response in different ways and distinctly influence inflammation, oxidative stress and blood coagulation according to their biochemical properties. In addition, an excess of other LE components, such as phospholipids and phytosterols, may be associated with hepatic steatosis and dysfunction. These associations do not represent direct risks or obstacles to LE use in metabolically stable patients but can render the choice of the best LE for hypermetabolic patients difficult. The infusion of LEs according to the available guidelines provides more benefit than harm and should be part of exclusive parenteral nutrition regimens or complement enteral nutrition when appropriate. The patient's metabolic profile should guide the type of FA and amount of lipids that are provided. For critically ill hypermetabolic patients, growing evidence indicates that standard LEs based solely on soybean oil should be avoided in favor of new LEs containing medium-chain triglycerides, olive oil, or fish oil to decrease the provision of potentially oxidative, inflammatory/immunosuppressive, and prothrombotic n-6 FAs. In addition, as sources of eicosapentaenoic and docosahexaenoic acids, LEs containing fish oil may be important for critically ill patients because they allow better modulation of the immune response and likely reduce the length of intensive care unity stay. However, current evidence precludes the recommendation of a specific LE for clinical use in this patient population. (C) 2015 S. Karger AG, Basel
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Referências
- Adolph M, 2009, GER MED SCI, V7
- Antébi H, 2004, JPEN J Parenter Enteral Nutr, V28, P142, DOI 10.1177/0148607104028003142
- Barbosa VM, 2010, CRIT CARE, V14, DOI 10.1186/cc8844
- Battistella FD, 1997, J TRAUMA, V43, P52, DOI 10.1097/00005373-199707000-00013
- Calder PC, 2010, INTENS CARE MED, V36, P735, DOI 10.1007/s00134-009-1744-5
- Calder PC, 2013, P NUTR SOC, V72, P263, DOI 10.1017/S0029665113001250
- Cano NJM, 2006, BRIT J NUTR, V95, P152, DOI 10.1079/BJN20051595
- Chen B, 2010, JPEN-PARENTER ENTER, V34, P387, DOI 10.1177/0148607110362532
- CLARKE PJ, 1987, BRIT J SURG, V74, P701, DOI 10.1002/bjs.1800740818
- Crimi E, 2006, FREE RADICAL BIO MED, V40, P398, DOI 10.1016/j.freeradbiomed.2005.10.054
- Demirer S, 2000, CLIN NUTR, V19, P253, DOI 10.1054/clnu.2000.0101
- Dhaliwal R, 2014, NUTR CLIN PRACT, V29, P29, DOI 10.1177/0884533613510948
- ELMADFA I, 1993, ANN NUTR METAB, V37, P8, DOI 10.1159/000177743
- Furukawa K, 2002, NUTRITION, V18, P235, DOI 10.1016/S0899-9007(01)00784-5
- Gelas P, 1998, JPEN-PARENTER ENTER, V22, P67, DOI 10.1177/014860719802200267
- Gobel Y, 2003, J PEDIATR GASTR NUTR, V37, P161, DOI 10.1097/00005176-200308000-00015
- GOGOS CA, 1994, J AM COLL NUTR, V13, P40
- Goulet O, 1999, AM J CLIN NUTR, V70, P338
- Grimm H, 2006, EUR J NUTR, V45, P55, DOI 10.1007/s00394-005-0573-8
- Han YY, 2012, NUTR CLIN PRACT, V27, P91, DOI 10.1177/0884533611429796
- Hardy G, 1997, NUTRITION, V13, P230, DOI 10.1016/S0899-9007(96)00040-8
- Jarstrand C, 1978, JPEN J Parenter Enteral Nutr, V2, P663, DOI 10.1177/0148607178002005663
- Klek S, 2013, CLIN NUTR, V32, P224, DOI 10.1016/j.clnu.2012.06.011
- Kuse ER, 2002, TRANSPLANT INT, V15, P272, DOI 10.1007/s00147-002-0393-1
- Laviano A, 2010, S AFR J CLIN NUTR, V23, pS08
- LOO LS, 1982, J INFECT DIS, V146, P64
- Manuel-y-Keenoy B, 2002, EUR J CLIN NUTR, V56, P121, DOI 10.1038/sj.ejcn.1601294
- Manzanares W, 2013, INTENS CARE MED, V39, P1683, DOI 10.1007/s00134-013-2999-4
- Manzanares W, 2014, JPEN-PARENTER ENTER, V38, P20, DOI 10.1177/0148607113486006
- Mateu-de Antonio Javier, 2008, Br J Nutr, V99, P846
- MEGUID MM, 1984, ARCH SURG-CHICAGO, V119, P1294
- Meguid M M, 1982, JPEN J Parenter Enteral Nutr, V6, P304, DOI 10.1177/0148607182006004304
- NORDENSTROM J, 1979, AM J CLIN NUTR, V32, P2416
- Onar P, 2011, NUTR CLIN PRACT, V26, P61, DOI 10.1177/0884533610392920
- PALUZZI M, 1987, SURGERY, V102, P711
- PORTA I, 1994, INFUSIONSTHERAPIE, V21, P316
- Pradelli L, 2012, CRIT CARE, V16, DOI 10.1186/cc11668
- Reimund JM, 2005, ALIMENT PHARM THERAP, V21, P445, DOI 10.1111/j.1365-2036.2005.02354.x
- Roulet M, 1997, JPEN-PARENTER ENTER, V21, P296, DOI 10.1177/0148607197021005296
- Schade I, 2008, CRIT CARE S2, V12, ps56
- SEDMAN PC, 1991, BRIT J SURG, V78, P1396, DOI 10.1002/bjs.1800781142
- Singer P, 2011, MINERVA ANESTESIOL, V77, P1115
- Siqueira J, 2011, J CLIN ENDOCR METAB, V96, P3207, DOI 10.1210/jc.2011-0480
- Staun M, 2009, CLIN NUTR, V28, P467, DOI 10.1016/j.clnu.2009.04.001
- Thomas-Gibson S, 2004, CLIN NUTR, V23, P697, DOI 10.1016/j.clnu.2003.11.007
- Trachootham D, 2008, ANTIOXID REDOX SIGN, V10, P1343, DOI 10.1089/ars.2007.1957
- Umpierrez GE, 2012, CRIT CARE MED, V40, P1792, DOI 10.1097/CCM.0b013e3182474bf9
- vanderPoll T, 1996, THROMB HAEMOSTASIS, V75, P83
- Verdier P, 2002, NUTR CLIN METAB, V16, P85, DOI 10.1016/S0985-0562(02)00115-2
- Waitzberg DL, 2009, NUTR CLIN PRACT, V24, P487, DOI 10.1177/0884533609339071
- Waitzberg DL, 2006, JPEN-PARENTER ENTER, V30, P351, DOI 10.1177/0148607106030004351
- Wang J, 2012, NUTRITION, V28, P623, DOI 10.1016/j.nut.2011.08.004
- Wichmann MW, 2007, CRIT CARE MED, V35, P700, DOI 10.1097/01.CCM.0000257465.60287.AC