Beta blockers in critical illness: promising but appropriate subphenotyping is needed

Luyao Zhang , Lu Ke

Burns & Trauma ›› 2024, Vol. 12 ›› Issue (1) : tkae060

PDF (448KB)
Burns & Trauma ›› 2024, Vol. 12 ›› Issue (1) :tkae060 DOI: 10.1093/burnst/tkae060
Commentary
research-article
Beta blockers in critical illness: promising but appropriate subphenotyping is needed
Author information +
History +
PDF (448KB)

Cite this article

Download citation ▾
Luyao Zhang, Lu Ke. Beta blockers in critical illness: promising but appropriate subphenotyping is needed. Burns & Trauma, 2024, 12 (1) : tkae060 DOI:10.1093/burnst/tkae060

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

Sanfilippo F, Santonocito C, Foëx P. Use of beta-blockers in non-cardiac surgery: an open debate. Minerva Anestesiol. 2014; 80: 482-94.

[2]

Heyland DK, Wibbenmeyer L, Pollack J, Friedman B, Turgeon AF, Eshraghi N, et al. A randomized trial of enteral glutamine for treatment of burn injuries. N Engl J Med. 2022; 387: 1001-10. https://doi.org/10.1056/NEJMoa2203364.

[3]

Hundeshagen G, Blears E, Mertin V, Day AG, Palackic A, Tapking C, et al. Administration and effects of beta blockers and oxandrolone in severely burned adults: a post hoc analysis of the RE-ENERGIZE trial. Burns Trauma. 2024; 12: tkad063. https://doi.org/10.1093/burnst/tkad063.

[4]

Pereira CT, Murphy KD, Herndon DN. Altering metabolism. J Burn Care Rehabil. 2005; 26: 194-9.

[5]

Clark A, Imran J, Madni T, Wolf SE. Nutrition and metabolism in burn patients. Burns Trauma. 2017; 5: 11. https://doi.org/10.1186/s41038-017-0076-x.

[6]

Chen J, Zhang D, Zhang J, Wang Y. Pathological changes in the brain after peripheral burns. Burns Trauma. 2023; 11: tkac061. https://doi.org/10.1093/burnst/tkac061.

[7]

Wilmore DW, Long JM, Mason AD Jr, Skreen RW, Pruitt BA Jr. Catecholamines: mediator of the hypermetabolic response to thermal injury. Ann Surg. 1974; 180: 653-69. https://doi.org/10.1097/00000658-197410000-00031.

[8]

Jeschke MG, Mlcak RP, Finnerty CC, Norbury WB, Gauglitz GG, Kulp GA, et al. Burn size determines the inflammatory and hypermetabolic response. Crit Care. 2007; 11: R90. https://doi.org/10.1186/cc6102.

[9]

Herndon DN, Hart DW, Wolf SE, Chinkes DL, Wolfe RR. Reversal of catabolism by beta-blockade after severe burns. N Engl J Med. 2001; 345: 1223-9. https://doi.org/10.1056/NEJMoa010342.

[10]

Herndon DN, Rodriguez NA, Diaz EC, Hegde S, Jennings K, Mlcak RP, et al. Long-term propranolol use in severely burned pediatric patients: a randomized controlled study. Ann Surg. 2012; 256: 402-11. https://doi.org/10.1097/SLA.0b013e318265427e.

[11]

Williams FN, Herndon DN, Kulp GA, Jeschke MG. Propranolol decreases cardiac work in a dose-dependent manner in severely burned children. Surgery. 2011; 149: 231-9. https://doi.org/10.1016/j.surg.2010.05.015.

[12]

Cheema SA, Ahmed UT, Nasir H, Dogar SR, Mustafa Z. Effects of propranolol in accelerating wound healing and attenuation of hypermetabolism in adult burn patients. J Coll Physicians Surg Pak. 2020; 30: 46-50. https://doi.org/10.29271/jcpsp.2020.01.46.

[13]

Rehou S, de Brito Monteiro L, Auger C, Knuth CM, Abdullahi A, Stanojcic M, et al. Propranolol normalizes Metabolomic signatures thereby improving outcomes after burn. Ann Surg. 2023; 278: 519-29. https://doi.org/10.1097/SLA.0000000000005973.

[14]

Yin J, Mao W, Xiao X, Yu X, Li B, Chen F, et al. Immune dysfunction is associated with readmission in survivors of sepsis following infected pancreatic necrosis. J Inflamm Res. 2021;Volume 14: 5433-42. https://doi.org/10.2147/JIR.S321507.

[15]

Zhang L, Zhou J, Ke L, Nie Y, Tong Z, Li W, et al. Role of heart rate variability in predicting the severity of severe acute pancreatitis. Dig Dis Sci. 2014; 59: 2557-64. https://doi.org/10.1007/s10620-014-3192-5.

[16]

Zhang L, Nie Y, Zheng Y, Ke L, Tong Z, Li W, et al. Esmolol attenuates lung injury and inflammation in severe acute pancreatitis rats. Pancreatology. 2016; 16: 726-32. https://doi.org/10.1016/j.pan.2016.05.395.

[17]

Morelli A, Ertmer C, Westphal M, Rehberg S, Kampmeier T, Ligges S, et al. Effect of heart rate control with esmolol on hemodynamic and clinical outcomes in patients with septic shock: a randomized clinical trial. JAMA. 2013; 310: 1683-91. https://doi.org/10.1001/jama.2013.278477.

[18]

Whitehouse T, Hossain A, Perkins GD, Gordon AC, Bion J, Young D, et al. Landiolol and organ failure in patients with septic shock: the STRESS-L randomized clinical trial. JAMA. 2023; 330: 1641-52. https://doi.org/10.1001/jama.2023.20134.

[19]

Kakihana Y, Ito T, Nakahara M, Yamaguchi K, Yasuda T. Sepsis-induced myocardial dysfunction: pathophysiology and management. J Intensive Care. 2016; 4: 22. https://doi.org/10.1186/s40560-016-0148-1.

[20]

Liaudet L, Calderari B, Pacher P. Pathophysiological mechanisms of catecholamine and cocaine-mediated cardiotoxicity. Heart Fail Rev. 2014; 19: 815-24. https://doi.org/10.1007/s10741-014-9418-y.

[21]

Boissier F, Aissaoui N. Septic cardiomyopathy: diagnosis and management. J Intensive Medicine. 2021; 2: 8-16. https://doi.org/10.1016/j.jointm.2021.11.004.

[22]

Hollenberg SM.β-Blockers in patients with sepsis: putting the puzzle together. Piece by Piece JAMA. 2023; 330: 1627-8. https://doi.org/10.1001/jama.2023.20455.

[23]

Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The third international consensus definitions for sepsis and septic shock (Sepsis-3). JAMA. 2016; 315: 801-10. https://doi.org/10.1001/jama.2016.0287.

PDF (448KB)

0

Accesses

0

Citation

Detail

Sections
Recommended

/

〈 〉