Miquet RLM, Escobar VH, Chávez MMÁ, Castañeda PA, Gutierrez RÁ, Posada RDA

Language: Spanish
References: 25
Page: 1-15
PDF size: 362.25 Kb.

ABSTRACT

Introduction: In burn disease, lipid metabolism is altered early. Total cholesterol is a biochemical indicator of nutritional status that could provide information on evolution.
Objective: To determine the state of total cholesterol and its tendency during the evolution of the burned patient.
Methods: A descriptive, longitudinal and prospective study was designed with 50 patients with burns classified from severe to extreme critical, with no other trauma or history of disease, treated at Hermanos Ameijeiras Clinical-Surgical Hospital and according to the established protocols. Total cholesterol level in blood was systematically determined after resuscitation and up to the sixth week, while such evolutionary trend was observed. Two groups were designed using 30 percent burned surface as a cut-off point. They were also analyzed according to chances of survival, the presence of major complications, and the condition at discharge. The data were summarized according to type of variable and relevant statistical tests were applied for their associations with a significance level of 0.05.
Results: Hypocholesterolemia was frequent. The longest extension and the worst prognosis were associated with significantly lower total cholesterol levels and a tendency to worsen; the latter was also significantly associated with the onset of major complications and death.
Conclusions: Burn disease produces hypocholesterolemia secondary to trauma and is associated with greatest extension, worst prognosis, onset of complications, and mortality. Total cholesterol could be a prognostic indicator in burns.

REFERENCES

1. Porter C, Tompkins RG, Finnerty CC, Sidossis LS, Suman OE, Herndon DN. The matabolic stress response to burns trauma: current understanding and therapies. Lancet. PubMed:PMID:27707498. 2016;388(10052):1417-26.

2. Barreto Penié J. Respuesta al ayuno, inanición y agresión. En: Anaya Prado R, Arenas Márquez H, Arenas Moya D, editores. Nutrición enteral parenteral. 2da ed. México DF: McGraw-Hill; 2012:9-17.

3. Birke G, Carlson LA. Lipid metabolism and trauma: plasma lipids and lipoproteins in burns. Acta Med Scand. 1965;168:337-50.

4. Coombes EJ, Shakespeare PG, Batstone GF. Lipoprotein changes after burn injury in man. J Trauma. 1980;20:971-5.

5. Miquet RL, Oseas LL, Rodríguez GR, Escobar VH. Hipocolesterolemia en el paciente quemado. Rev. Acta Médica. 2016;17(2)

6. Vanni HE, Gordon BR, Levine DM. Cholesterol and interleukin-6 concentrations related to out comes in burn injured patients. J Burn Care Rehabil. 2003;24(3):133-41.

7. Ogunbilege J, Porter C, Herdon D, Chao T. Abdelrahman D, Papadimitriou A, et al. Hypermetabolism and hypercatabolism of skeletal muscle accompany mitochondrial stress following severe burns trauma. AM J Physiol Endocrinol Metab. 2016;311:436-48.

8. Moreira E, Burghi GY, Manzanares W. Nutrition in burns patient. J Mahatma Gandhi Inst Med Sci. 2016;21:8-11.

9. Moreira E, Burghi G, Manzanares W: Metabolismo y terapia nutricional en el paciente quemado crítico: una revisión actualizada. Med. Intens. 2018;42(5):306-16.

10. Borges MH, García RR. Manual de procedimientos de diagnóstico y tratamiento en caumatología y cirugía plástica. La Habana: Editorial Pueblo y Educación; 1984.

11. Auger CT et al. The biochemical alterations underlying post-burns hypermetabolism, Biochimica et Biophysica. Acta. 2017;1863(10):2633-44.

12. Yamano S, Shimizu K, Ogura H, et al. Low total cholesterol and high total bilirubin are associated with prognosis in patients with prolonged sepsis. Journal of Critical Care. 2016;31(1):36-40.

13. Chien YF, Chen CY, Hsu CL, Chen KY, Yu CJ. Decreased serum level of lipoprotein cholesterol is a poor prognostic factor for patients with severe community-acquired pneumonia that required intensive care unit admission: PubMed.PMID:25702844. J Crit Care. 2015;30(3):506-10.

14. Morin EE, GuoL, Schwendeman A, An LiX.HDL in sepsis _risk factor and therapeutic approach. Front Pharmacol. 2015;6:244.

15. Sharpe LJ, Burns V, Brown AJ. Alipidomic perspective on intermediates in cholesterol synthesis as indicators of disease status. J Genet Genomics. 2014;41(5):275-82.

16. Nielson CB, Duethman NC, Howard JM, Moncure M, Wood JG. Burns: Pathophysiology of Sustemic complications and currente management. J Burn Care Res.2017;38(1):469-81.

17. Kaddour I, Abu-Sittah G, Ibraim A, Karamanoukian R, Papazian N. Burn injury: review of pathophysiology and therapeutic modalities in major burns. Annals of burns and Fire Disasters. 2017;30(2):95-102.

18. Williams NF, Herdon ND.Metabolic and endocrine considerations after burn injury. Clin Plast. Surg. 2017;44 (3):541-53.

19. Chiarla C, Giovannini I, Giuliante F, Zadak Z, Vellone M, Ardito F, et al. Severe hypocholesterolemia in surgical patients, sepsis, and critical illness. J Crit Care. 2010;25(2):361.e7-361.e12.

20. Kamolz LP, Andel H, Mittlboeck M, Winter W, Haslik W, MeisslG. Serum cholesterol and triglycerides: potential role in mortality prediction. Burns. 2003;29:810.

21. Lee SH, Hong TH, Kim BO, LeeYJ. Severe hpersistent hypocholesterolemia after emergency gastrointestinal surgery predicts in-hospital mortality in critically ill patients with diffuse peritonitis. PloS ONE 2018;13(7):e0200187. https://doi.org/10.1371.journal.pone.0200187

22. Miquet RL, Rodríguez GR, González RH: Gran Quemado Adulto. Terapia Nutricional. Manual de Prácticas Médicas. Hospital Clínico Quirúrgico “Hermanos Ameijeiras”. VI edición. La Habana; 2018.

23. Sinwar PD. Nutrition in burns patient. J Mahatma Gandhi Inst Med Sci, 2016;21:8-11.

24. Barlage S, Gnewuch C, Liebisch G, Wolf Z, Audebert FX, Glück T, et al. Changes in HDL-associated apolipoproteins relate to mortality in human sepsis and correlate to monocyte and platelet activation. Intensive Care Med. 2009;35(11):1877-85.

25. Biller K, Fae P, Germann R, Drexel H, Walli AK, Fraunberger P. Cholesterol rather than procalcitonin or C-reactive protein predicts mortality in patients with infection. Shock. 2014;42(2):129-32.