Sepsis-induced damage to endothelial glycocalyx (literature review)

Y.Y. Ilyina, E.V. Fot, V.V. Kuzkov, M.Y. Kirov

Department of Anesthesiology, City Hospital No 1, Arkhangelsk

Department of Anesthesiology and Intensive Care, Northern State Medical University, Arkhangelsk

For correspondence: Yana Y. Ilyina, Department of Anesthesiology and Intensive Care, Northern State Medical University, Arkhangelsk; e-mail: yana.ilyina@mail.ru

For citation: Ilyina YY, Fot EV, Kuzkov VV, Kirov MY. Sepsis-induced damage to endothelial glycocalyx (literature review). Alexander Saltanov Intensive Care Herald. 2019;2:2-39.

DOI: 10.21320/1818-474X-2019-2-32-39


Glycocalyx is a gel-like layer covering the surface of vascular endothelial cells. It consists of membrane-attached proteoglycans, glycosaminoglycan chains, glycoproteins, and plasma adhesive proteins. Glycocalyx plays a key role in maintaining vascular homeostasis, controls vascular permeability and the tone of the microvasculature, prevents microvascular thrombosis and regulates leukocyte adhesion. In sepsis and septic shock, damage and shedding of glycocalyx occurs. The degradation of glycocalyx is activated by reactive oxygen species and pro-inflammatory cytokines, such as tumor necrosis factor (TNF) and interleukin-1β (IL-1β). The inflammation-mediated degradation of glycocalyx leads to vascular hyperpermeability, unregulated vasodilation, microvascular thrombosis, and enhanced leukocyte adhesion. The inflammation-mediated degradation of glycocalyx leads to vascular hyperpermeability, unregulated vasodilation, microvascular thrombosis, and enhanced leukocyte adhesion. Clinical studies have demonstrated a correlation between the levels of glycocalyx components in the blood and organ dysfunction and mortality in sepsis and septic shock. Inflammation-induced damage to glycocalyx can cause a number of specific clinical effects of sepsis, including acute kidney damage, respiratory failure and liver dysfunction. Infusion therapy is an integral part of the treatment of sepsis, but super-aggressive infusion load methods (leading to hypervolemia) may increase the degradation of glycocalyx. Moreover, some markers of glycocalyx degradation, such as circulating levels of syndecan 1 or heparan sulfate, can be used as markers of endothelial dysfunction and sepsis severity.

Keywords: endothelial glycocalyx, endothelium, sepsis, septic shock, glycocalyx shedding, vascular permeability

Received: 08.02.2019


References

  1. Uchimido R., Schmidt E.P., Shapiro N.I. The glycocalyx: a novel diagnostic and therapeutic target in sepsis. Crit. Care. 2019; 23: 16. DOI: 10.1186/s13054-018-2292-6
  2. Colbert J.F., Schmidt E.P. Endothelial and microcirculatory function and dysfunction in sepsis. Clin. Chest. Med. 2016; 37: 263–275. DOI: 10.1016/j.ccm.2016.01.009
  3. Максименко А.В. Эндотелиальный гликокаликс — значимая составная часть двойного защитного слоя сосудистой стенки: диагностический индикатор и терапевтическая мишень. Кардиологический вестник. 2016; 11(3): 94–100. [Maksimenko A.V. endothelial glygogalyx is significant constitutive part of double protective layer into vascular wall: diagnostic index and therapeutic target. Kardiologicheskij Vestnik. 2016; 11(3): 94–100. (In Russ)]
  4. Гончар И.В., Балашов С.А.,. Валиев И.А., Мелькумянц А.М. Роль эндотелиального гликокаликса в механогенной регуляции тонуса артериальных сосудов. Труды московского физико-химического института. 2017; 1: 101–108. [Gonchar I.V., Balashov S.A., Valiev I.A., Melkumyanz А.М. The role of endothelial glycocalyx in the mechanogenic regulation of arterial vascular tone. Proceedings of the Moscow Institute of Physics and Chemistry. 2017; 1: 101–108. (In Russ)]
  5. Woodcock T.E., Woodcock T.M. Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy. Br. J. Anaesth. 2012; 108: 384–394. DOI: 10.1093/bja/aer515
  6. Frati-Munari A.C. Medical significance of endothelial glycocalyx. Arch Cardiol Mex. 2013; 83: 303–312. DOI: 10.1016/j.acmx.2013.04.015
  7. Kolářová H., Ambrůzová B., Svihálková L., et al. Modulation of endothelial glycocalyx structure under inflammatory conditions. Mediators Inflamm. 2014: ID 694312. DOI: 10.1155/2014/694312
  8. Singh A., Ramnath R.D., Foster R.R., et al. Reactive oxygen species modulate the barrier function of the human glomerular endothelial glycocalyx. PLoS One. 2013; 8(1): e55852. DOI: 10.1371/journal.pone.0055852
  9. Stehouwer C.D., Smulders YM. Microalbuminuria and risk for cardiovascular disease: analysis of potential mechanisms. J. Am. Soc. Nephrol. 2006; 17: 2106–2111. DOI: 10.1681/ASN.2005121288
  10. Forbes J.M., Coughlan M.T., Cooper ME. Oxidative stress as a major culprit in kidney disease in diabetes. Diabetes. 2008; 57: 1446–1454. DOI: 10.2337/db08–0057
  11. Adachi T., Fukushima T., Usami Y., et al. Binding of human xanthine oxidase to sulphated glycosaminoglycans on the endothelial-cell surface. Biochem J. 1993; 289: 523–527. DOI: 10.1042/bj2890523
  12. Becker M., Menger M.D., Lehr H.A. Heparin-released superoxide dismutase inhibits postischemic leukocyte adhesion to venular endothelium. Am. J. Physiol. 1994; 267: 925–930. DOI: 10.1152/ajpheart.1994.267.3.H925
  13. Becker B.F., Chappell D., Bruegger D., et al. Therapeutic strategies targeting the endothelial glycocalyx: acute deficits, but great potential. Cardiovasc. Res. 2010; 87: 300–310. DOI: 10.1093/cvr/cvq137
  14. Gouverneur M., Spaan J.A., Pannekoek H., et al. Fluid shear stress stimulates incorporation of hyaluronan into endothelial cell glycocalyx. American Journal of Physiology. Heart and Circulatory Physiology. 2006; 290: 458–462. DOI: 10.1152/ajpheart.00592.2005
  15. Johansson P.I., Henriksen H.H., Stensballe J., et al. Traumatic endotheliopathy: a prospective observational study of 424 severely injured patients. Ann. Surg. 2017; 265(3): 597–603. DOI: 10.1097/SLA.0000000000001751
  16. Gandhi N.S., Mancera R.L. The structure of glycosaminoglycans and their interactions with proteins. Chem. Biol. Drug. Des. 2008; 72(6): 455–482. DOI: 10.1111/j.1747-0285.2008.00741.x
  17. Paulus P., Jennewein C., Zacharowski K. Biomarkers of endothelial dysfunction: can they help us deciphering systemic inflammation and sepsis? Biomarkers. 2011; 16: 11–21. DOI: 10.3109/1354750X.2011.587893
  18. Reitsma S., Slaaf D.W., Vink H., et al. The endothelial glycocalyx: composition, functions, and visualization. Pflugers Archiv: European Journal of Physiology. 2007; 454: 345–359. DOI: 10.1007/s00424-007-0212-8
  19. Rehm M., Bruegger D., Christ F., et al. Shedding of the endothelial glycocalyx in patients undergoing major vascular surgery with global and regional ischemia. Circulation. 2007; 116: 1896–1906. DOI: 10.1161/circulationaha.106.684852
  20. Burke-Gaffney A., Evans T.W. Lest we forget the endothelial glycocalyx in sepsis. Crit. Care. 2012; 16: 121. DOI: 10.1186/cc11239
  21. Kozar R.A., Peng Z., Zhang R., et al. Plasma restoration of endothelial glycocalyx in a rodent model of hemorrhagic shock. Anesth. Analg. 2011; 112: 1289–1295. DOI: 10.1213/ANE.0b013e318210385c
  22. Cancel L.M., Ebong E.E., Mensah S., et al. Endothelial glycocalyx, apoptosis and inflammation in an atherosclerotic mouse model. Atherosclerosis. 2016; 252: 136–146. DOI: 10.1016/j.atherosclerosis.2016.07.930
  23. Miranda C.H., de Carvalho Borges M., Schmidt A., et al. Evaluation of the endothelial glycocalyx damage in patients with acute coronary syndrome Atherosclerosis. 2016; 247: 184–188. DOI: 10.1016/j.atherosclerosis.2016.02.023
  24. Padberg J.S., Wiesinger A., di Marco G.S. Damage of the endothelial glycocalyx in chronic kidney disease. Atherosclerosis. 2014; 234: 335–343. DOI: 10.1016/j.atherosclerosis.2014.03.016
  25. Nieuwdorp M., Mooij H.L., Kroon J., et al. Endothelial glycocalyx damage coincides with microalbuminuria in type 1 diabetes. Diabetes. 2006; 55: 1127–1132. DOI: 10.2337/diabetes.55.04.06.db05–1619
  26. Jacob M., Saller T., Chappell D., et al. Physiological levels of A-, B- and C-type natriuretic peptide shed the endothelial glycocalyx and enhance vascular permeability. Basic Res Cardiol. 2013; 108: 347. DOI: 10.1007/s00395-013-0347-z
  27. Salmon A.H., Satchell S.C. Endothelial glycocalyx dysfunction in disease: albuminuria and increased microvascular permeability. J. Pathol. 2012; 226: 562–574. DOI: 10.1002/path.3964
  28. Myburgh J.A., Mythen M.G. Resuscitation fluids. N. Engl. J. Med.. 2013; 369: 1243–1251.
  29. Henrich M., Gruss M., Weigand M.A. Sepsis-induced degradation of endothelial glycocalyx. Sci World J. 2010; 10: 917–923. DOI: 10.1100/tsw.2010.88
  30. Bruegger D., Jacob M., Rehm M. Atrial natriuretic peptide induces shedding of the endothelial glycocalyx in the coronary vascular bed of guinea pig. Am. J. Physiol. Heart Circ. Physiol. 2005; 289: 1993–1999. DOI: 10.1152/ajpheart.00218.2005
  31. Adamson R.H., Lenz J.F., Zhang X., et al. Oncotic pressures opposing filtration across non-fenestrated rat microvessels. Journal of Physiology. 2004; 557: 889–907. DOI: 10.1113/jphysiol.2003.058255
  32. Levick J.R., Michel C.C. Microvascular fluid exchange and the revised Starling principle. Cardiovascular Research. 2010; 87: 198–210. DOI: 10.1093/cvr/cvq062
  33. Ait-Oufella H., Maury E., Lehoux S., et al. The endothelium: physiological functions and role in microcirculatory failure during severe sepsis. Intensive Care Medicine. 2010; 36: 1286–1298. DOI: 10.1007/s00134-010-1893-6
  34. Pries A.R., Secomb T.W., Gaehtgens P. The endothelial surface layer. Pflugers Arch. 2000; 440: 653–666. DOI: 10.1007/s004240000307
  35. Jacob M., Bruegger D., Rehm M., et al. The endothelial glycocalyx affords compatibility of Starlingʼs principle and high cardiac interstitial albumin levels. Cardiovascular Research. 2007; 73: 575–586. DOI: 10.1016/j.cardiores.2006.11.021
  36. Florian J.A., Kosky J.R., Ainslie K., et al. Heparan sulfate proteoglycan is a mechanosensor on endothelial cells. Circ. Res. 2003; 93: 136–142. DOI: 10.1161/01.RES.0000101744.47866.D5
  37. Chelazzi C., Villa G., Mancinelli P., et al. Glycocalyx and sepsis-induced alterations in vascular permeability. Crit. Care. 2015; 19: 26. DOI: 10.1186/s13054-015-0741-z
  38. Karamysheva A.F. Mechanisms of angiogenesis. Biochemistry. 2008; 73: 751–762.
  39. Becker B.F., Jacob M., Leipert S., et al. Degradation ot the endothelial glycocalyx in clinical settings: searching for the sheddases. Br. J. Clin Pharmacol. 2015; 80: 389–402. DOI: 10.1111/bcp.12629
  40. Moseley R., Waddington R.J., Embery G. Degradation of glycosaminoglycans by reactive oxygen species derived from stimulated polymorphonuclear leukocytes. Biochim. Biophys. Acta. 1997; 1362: 221. DOI: 10.1016/S0925–4439(97)00083–5
  41. Weinbaum S., Tarbell J.M., Damiano E.R. The structure and function of the endothelial glycocalyx layer. Annu Rev. Biomed. Eng. 2007; 9: 121–167. DOI: 10.1146/annurev.bioeng.9.060906.151959
  42. Forni M., Mazzola S., Ribeiro L.A., et al. Expression of endothelin-1 system in a pig model of endotoxic shock. Regul. Pept. 2005; 131: 89–96. DOI: 10.1016/j.regpep.2005.07.001
  43. Johansson P., Stensballe J., Ostrowski S. Shock induced endotheliopathy (SHINE) in acute critical illness — a unifying pathophysiologic mechanism. Crit. Care. 2017; 21: 25. DOI: 10.1186/s13054-017-1605-5
  44. Johansson P.I., Stensballe J., Rasmussen L.S., et al. A high admission syndecan-1 level, a marker of endothelial glycocalyx degradation, is associated with inflammation, protein C depletion, fibrinolysis, and increased mortality in trauma patients. Ann. Surg. 2011; 254: 194–200. DOI: 10.1097/SLA.0b013e318226113d
  45. Steppan J., Hofer S., Funke B. Sepsis and major abdominal surgery lead to flaking of the endothelial glycocalyx. J. Surg. Res. 2011; 165: 136–141. DOI: 10.1016/j.jss.2009.04.034
  46. Ostrowski S.R., Gaïni S., Pedersen C.J., et al. Sympathoadrenal activation and endothelial damage in patients with varying degrees of acute infectious disease: An observational study. Crit. Care. 2015; 30: 90–96. DOI: 10.1016/j.jcrc.2014.10.006
  47. Haywood-Watson R.J., Holcomb J.B., Gonzalez E.A., et al. Modulation of syndecan-1 shedding after hemorrhagic shock and resuscitation. PLoS One. 2011; 6 (8): e23530. DOI: 10.1371/journal.pone.0023530
  48. Aird W.C. Endothelial cell heterogeneity. Cold Spring Harb Perspect Med. 2012; 2: a006429. DOI: 10.1101/cshperspect.a006429
  49. Ince C., Mayeux P.R., Nguyen T. The endothelium in sepsis shock. Shock. 2016; 45(3): 259–270. DOI: 10.1097/SHK.0000000000000473
  50. Zeng Y., Adamson R.H., Curry F.R.E., et al. Sphingosine-1-phosphate protects endothelial glycocalyx by inhibiting syndecan-1 shedding. Am. J. Physiol. Heart Circ. Physiol. 2014; 306: H363–H372. DOI: 10.1152/ajpheart.00687.2013
  51. Coldewey S. M, Benetti E., Collino M., et al. Elevation of serum sphingosine-1-phosphate attenuates impaired cardiac function in experimental sepsis. Sci Rep. 2016; 6: 27594. DOI: 10.1038/srep27594.
  52. Schmidt E.P, Yang Y., Janssen W.J., et al. The pulmonary endothelial glycocalyx regulates neutrophil adhesion and lung injury during experimental sepsis. Nat. Med. 2012; 18: 1217–1223. DOI: 10.1038/nm.2843
  53. Purushothaman A., Chen L., Yang Y., et al. Heparanase stimulation of protease expression implicates it as a master regulator of the aggressive tumor phenotype in myeloma. J. Biol. Chem. 2008; 283: 32628–32636. DOI: 10.1074/jbc.M806266200
  54. Masola V., Onisto M., Zaza G., et al. A new mechanism of action of sulodexide in diabetic nephropathy: inhibits heparanase-1 and prevents FGF-2-induced renal epithelial-mesenchymal transition. J. Transl. Med. 2012; 10: 213. DOI: 10.1186/1479-5876-10-213
  55. Song J.W., Zullo J.A., Liveris D., et al. Therapeutic restoration of endothelial glycocalyx in sepsis. J. Pharmacol. Exp. Ther. 2017; 361: 115–121. DOI: 10.1124/jpet.116.239509
  56. Yang Y., Haeger S.M., Suflita M.A., et al. Fibroblast growth factor signaling mediates pulmonary endothelial glycocalyx reconstitution. Am. J. Respir. Cell Mol. Biol. 2017; 56: 727–737. DOI: 10.1165/rcmb.2016–0338OC
  57. Rizzo A. N, Dudek S.M. Endothelial glycocalyx repair: building a wall to protect the lung during sepsis. Am. J. Respir. Cell Mol. Biol. 2017; 56: 687–688. DOI: 10.1165/rcmb.2017–0065ED
  58. Frati-Munari A.C. Medical significance of endothelial glycocalyx. Arch. Cardiol. Mex. 2013; 83: 303–312. DOI: 10.1016/j.acmx.2013.04.015
  59. Nieuwdorp M., van Haeften T.W., Gouverneur M.C., et al. Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo. Diabetes. 2006; 55: 480–486. DOI: 10.2337/diabetes.55.02.06.db05-1103
  60. Bruegger D., Schwartz L., Chappell D., et al. Release of atrial natriuretic peptide precedes shedding of the endothelial glycocalyx equally in patients undergoing on- and off-pump coronary artery bypass surgery. Basic Res. Cardiol. 2011; 106: 1111–1121.
  61. Adamson R.H., Clark J.F., Radeva M., et al. Albumin modulates S1P delivery from red blood cells in perfused microvessels: mechanism of the protein effect. Am. J. Physiol. Heart Circ. Physiol. 2014; 306: 1011–1017. DOI: 10.1152/ajpheart.00829.2013
  62. Jacob M., Bruegger D., Rehm M., et al.Contrasting effects of colloid and crystalloid resuscitation fluids on cardiac vascular permeability. Anesthesiology. 2006; 104: 1223–1231.
  63. Jacob M., Paul O., Mehringer L., et al. Albumin augmentation improves condition of guinea pig hearts after 4 hr of cold ischemia. Transplantation. 2009; 87: 956–965. DOI: 10.1097/TP.0b013e31819c83b5
  64. Torres L.N., Sondeen J.L., Ji L., et al. Evaluation of resuscitation fluids on endothelial glycocalyx, venular blood flow, and coagulation function after hemorrhagic shock in rats. J. Trauma Acute Care Surg. 2013; 75: 759–766. DOI: 10.1097/TA.0b013e3182a92514
  65. Peng Z., Pati S., Potter D., et al. Fresh frozen plasma lessens pulmonary endothelial inflammation and hyperpermeability after hemorrhagic shock and is associated with loss of syndecan 1. Shock. 2013; 40: 195–202. DOI: 10.1097/SHK.0b013e31829f91fc
  66. Haywood-Watson R.J., Holcomb J.B., Gonzalez E.A., et al. Modulation of syndecan-1 shedding after hemorrhagic shock and resuscitation. PLoS One. 2011; 6: e23530. DOI: 10.1371/journal.pone.0023530
  67. Straat M., Müller M.C., Meijers J.C., et al. Effect of transfusion of fresh frozen plasma on parameters of endothelial condition and inflammatory status in non-bleeding critically ill patients: a prospective substudy of a randomized trial. Crit. Care. 2015; 19: 62–67. DOI: 10.1186/s13054-015-0828-6
  68. Chappell D., Hofmann-Kiefer K., Jacob M., et al. TNF-alpha induced shedding of the endothelial glycocalyx is prevented by hydrocortisone and antithrombin. Basic Res. Cardiol. 2009; 104: 78–89.
  69. De Backer D., Creteur J., Preiser J.C. Microvascular blood flow is altered in patients with sepsis. Am. J. Respir. Crit. Care Med. 2002; 166: 98–104. DOI: 10.1164/rccm.200109–016OC

Nosocomial pneumonia — principles of early diagnosis and prevention

A.N. Kuzovlev, V.V. Moroz

Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow

For correspondence: Artem N. Kuzovlev, MD, DrMed, vice-director for science, head of the laboratory of clinical pathophysiology of critical states of the V.A. Negovsky research institute of general reanimatology Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow; e-mail: artem_kuzovlev@mail.ru

For citation: Kuzovlev AN, Moroz VV. Nosocomial pneumonia — principles of early diagnosis and prevention. Alexander Saltanov Intensive Care Herald. 2019;2:40-47.

DOI: 10.21320/1818-474X-2019-2-40-47


Nosocomial pneumonia and nosocomial tracheobronchitis present an urgent problem of anesthesiology and critical care medicine. This review presents the results of our own research on the informativity of new molecular biomarkers in the early diagnosis of nosocomial pneumonia, as well as modern principles for the prevention of nosocomial pneumonia. A promising direction for the early diagnosis of nosocomial pneumonia and its complications is the study of new molecular biomarkers, in particular, Clara cell protein and surfactant proteins. Effective prevention of nosocomial pneumonia should be based on a complex of modern evidence-based methods.

Keywords: nosocomial pneumonia, nosocomial tracheobronchitis, biomarkers, prophylaxis, sepsis, antibiotics, inhalation

Received: 23.02.2019


References

  1. Гельфанд Б.Р. Нозокомиальная пневмония у взрослых. Российские национальные рекомендации. М.: МИА, 2016.[Gelfand B.R. Nozokomialʼnaya pnevmoniya u vzroslyh. Rossijskie nacionalʼnye rekomendacii. M.: MIA, 2016. (In Russ)]
  2. Яковлев С.В., Суворова М.П., Белобородов В.Б., Басин Е.Е., Елисеева Е.В., Ковеленов С.В, и члены исследовательской группы ЭРГИНИ. Распространенность и клиническое значение нозокомиальных инфекций в лечебных учреждениях России: исследование ЭРГИНИ. Антибиотики и химиотерапия. 2016; 61(5–6): 32–42.[Yakovlev S.V., Suvorova M.P., Beloborodov V.B., Basin E.E., Eliseeva E.V., Kovelenov S.V, i chleny issledovatelʼskoj gruppy ERGINI. Rasprostranennostʼ i klinicheskoe znachenie nozokomialʼnyh infekcij v lechebnyh uchrezhdeniyah Rossii: issledovanie ERGINI. Antibiotiki i himioterapiya 2016; 61(5–6): 32–42. (In Russ)]
  3. Кузовлев А.Н., Шабанов А.К., Тюрин И.А. Динамика концентрации ингаляционного тобрамицина в крови и бронхоальвеолярной лаважной жидкости при нозокомиальной пневмонии (предварительное сообщение). Общая реаниматология. 2018; 14(5): 32–37. DOI: 10.15360/1813-9779-2018-5-32-37. [Kuzovlev A.N., Shabanov A.K., Tyurin I.A. Dinamika koncentracii ingalyacionnogo tobramicina v krovi i bronhoalʼveolyarnoj lavazhnoj zhidkosti pri nozokomialʼnoj pnevmonii (predvaritelʼnoe soobshchenie). Obshchaya reanimatologiya. 2018; 14(5): 32–37. DOI: 10.15360/1813-9779-2018-5-32-37. (In Russ)]
  4. Klompas M., Kleinman K., Murphy M. Descriptive epidemiology and attributive morbidity of ventilator-associated events. Infect. Control.Hosp. Epidemiol. 2014; 35(5): 502–510. DOI: 10.1086/675834
  5. Дмитриева Н.В., Петухова И.Н. Послеоперационные инфекционные осложнения. Практическое руководство. М.: Практическая медицина, 2013.[Dmitrieva N.V., Petuhova I.N. Posleoperacionnye infekcionnye oslozhneniya. Prakticheskoe rukovodstvo. Moscow: Prakticheskaya medicina, 2013. (In Russ)]
  6. Josefson P., Stralin K., Ohlin A., et al. Evaluation of a commercial multiplex PCR test (SeptiFast) in the etiological diagnosis of community-onset bloodstream infections. Eur. J. Clin. Microbiol. Infect. Dis. 2011; 30(9): 1127–1134. DOI: 10.1007/s10096-011-1201-6
  7. Мороз В.В., Голубев А.М., Кузовлев А.Н., Писарев В.М. Новые диагностические кандидатные молекулярные биомаркеры острого респираторного дистресс-синдрома. Общая реаниматология. 2014; 10(4): 6–10. DOI: 10.15360/1813-9779-2014-4-6-10. [Moroz V.V., Golubev A.M., Kuzovlev A.N., Pisarev V.M. Novye diagnosticheskie kandidatnye molekulyarnye biomarkery ostrogo respiratornogo distress-sindroma. Obshchaya reanimatologiya. 2014; 10(4): 6–10. DOI: 10.15360/1813-9779-2014-4-6-10. (In Russ)]
  8. Hayashida S, Harrod K.S., Whitsett J.A. Regulation and function of CCSP during pulmonary Pseudomonas aeruginosa infection in vivo. Am. J. Physiol. Lung. Cell. Mol. Physiol. 2000. 279(3): 452–459.
  9. Clara M. Zur Histobiologie des Bronchalepithels. [On the histobiology of the bronchial epithelium.]. Z mikrosk. Anat. Forsch. 1937; 41: 321–334.
  10. Policard A., Collet A., Giltaire-Ralyte L. Observations microélectroniques sur lʼinfrastructure des cellules bronchiolaires. [Electron microscopic observations on the ultrastructure of bronchiolar cells.] Les Bronches. 1955; 5: 187–196.
  11. Singh G., Katyal S.L. An immunologic study of the secretory products of rat Clara cells. J. Histochem. Cytochem. 1984; 32: 49–54.
  12. Snyder J., Reynolds S., Hollingsworth J., et al. Clara cells attenuate the inflammatory response through regulation of macrophage behavior. Am. J. Respir. Cell Mol. Biol. 2010; 42(2): 161–171. DOI: 10.1165/rcmb.2008–0353OC
  13. Determann R., Wolthuis E., Choi G., Bresser P., et al. Lung epithelial injury markers are not influenced by Use of Lower Tidal Volumes during Elective Surgery in Patients without Pre-existing Lung Injury. Am. J. Physiol. Lung. Cell Mol. Physiol. 2008; 294: 344–350.
  14. Negrin L.L., Halat G., Kettner S., et al. Club cell protein 16 and cytokeratin fragment 21–1 as early predictors of pulmonary complications in polytraumatized patients with severe chest trauma. PLoS One. 2017; 12(4): e0175303. DOI: 10.1371/journal.pone.0175303
  15. Lin J., Zhang W., Wang L., Tian F. Diagnostic and prognostic values of Club cell protein 16 (CC16) in critical care patients with acute respiratory distress syndrome. J. Clin. Lab. Anal. 2018; 32(2): DOI: 10.1002/jcla.22262
  16. Sorensen G.L. Surfactant Protein D in Respiratory and Non-Respiratory Diseases. Front. Med. (Lausanne). 2018; 5: 18. DOI: 10.3389/fmed.2018.00018
  17. Мороз В.В., Голубев А.М., Кузовлев А.Н. и др. Сурфактантный протеин D — биомаркер острого респираторного дистресс-синдрома. Общая реаниматология. 2013; 9(4): 11. DOI: 10.15360/1813-9779-2013-4-11. [Moroz V.V., Golubev A.M., Kuzovlev A.N., et al. Surfaktantnyj protein D — biomarker ostrogo respiratornogo distress-sindroma. Obshchaya reanimatologiya. 2013; 9(4): 11. DOI: 10.15360/1813-9779-2013-4-11. (In Russ)]
  18. King B., Kingma P. Surfactant Protein D Deficiency Increases Lung Injury during Endotoxemia. Am. J. Respir. Cell Mol. Biol. 2011; 44(5): 709–715. DOI: 10.1165/rcmb.2009–0436OC
  19. Said A., Abd-Elaziz M., Farid M., et al. Evolution of surfactant protein-D levels in children with ventilator-associated pneumonia. Pediatr Pulmonol. 2012; 47(3); 292–299. DOI: 10.1002/ppul.21548
  20. Tekerek N.U., Akyildiz B.N., Ercal B.D., Muhtaroglu S. New Biomarkers to Diagnose Ventilator Associated Pneumonia: Pentraxin 3 and Surfactant Protein D. Indian J. Pediatr. 2018; 85(6): 426–432. DOI: 10.1007/s12098-018-2607-2
  21. Park J., Pabon M., Choi A.M.K., et al. Plasma surfactant protein-D as a diagnostic biomarker for acute respiratory distress syndrome: validation in US and Korean cohorts. BMC Pulm. Med. 2017; 17(1): 204. DOI: 10.1186/s12890-017-0532-1
  22. Timsit J.F., Esaied W., Neuville M., et al. Update on ventilator-associated pneumonia. F1000Res. 2017; 6: 2061. DOI: 10.12688/f1000research.12222.1
  23. Reignier J., Darmon M., Sonneville R., et al. Impact of early nutrition and feeding route on outcomes of mechanically ventilated patients with shock: a post hoc marginal structural model study. Intensive Care Med. 2015; 41(5): 875–886. DOI: 10.1007/s00134-015-3730-4
  24. Fitch Z.W., Whitman G.J. Incidence, risk, and prevention of ventilator-associated pneumonia in adult cardiac surgical patients: a systematic review. J. Card. Surg. 2014; 29(2): 196–203. DOI: 10.1111/jocs.12260
  25. Schwebel C., Clecʼh C., Magne S., et al. Safety of intrahospital transport in ventilated critically ill patients: a multicenter cohort study. Crit. Care Med. 2013; 41(8): 1919–1928. DOI: 10.1097/CCM.0b013e31828a3bbd
  26. Bornstain C., Azoulay E., De Lassence A., et al. Sedation, sucralfate, and antibiotic use are potential means for protection against early-onset ventilator-associated pneumonia. Clin. Infect. Dis. 5; 38(10): 1401–1408.
  27. Rello J., Lode H., Cornaglia G., et al. A European care bundle for prevention of ventilator-associated pneumonia. Intensive Care Med. 2010; 36(5): 773–780. DOI: 10.1007/s00134-010-1841-5
  28. Bouadma L., Deslandes E., Lolom I., et al. Long-term impact of a multifaceted prevention program on ventilator-associated pneumonia in a medical intensive care unit. Clin Infect Dis. 2010; 51(10): 1115–1122. DOI: 10.1086/656737
  29. Muscedere J., Sinuff T., Heyland D.K., et al. The clinical impact and preventability of ventilator-associated conditions in critically ill patients who are mechanically ventilated. Chest. 2013; 144(5): 1453–1460. DOI: 10.1378/chest.13-0853
  30. Morris A.C., Hay A.W., Swann D.G., et al. Reducing ventilator-associated pneumonia in intensive care: impact of implementing a care bundle. Crit. Care Med. 2011; 39(10): 2218–2224. DOI: 10.1097/CCM.0b013e3182227d52
  31. Speck K., Rawat N., Weiner N.C., et al. A systematic approach for developing a ventilator-associated pneumonia prevention bundle. Am. J. Infect. Control. 2016; 44(6): 652–656. DOI: 10.1016/j.ajic.2015.12.020
  32. Oostdijk E.A.N., Kesecioglu .J, Schultz M.J., et al. Effects of decontamination of the oropharynx and intestinal tract on antibiotic resistance in ICUs: a randomized clinical trial. JAMA. 2014; 312(14): 1429–1437. DOI: 10.1001/jama.2014.7247
  33. Rabello F., Araújo V.E., Magalhães S. Effectiveness of oral chlorhexidine for the prevention of nosocomial pneumonia and ventilator-associated pneumonia in intensive care units: Overview of systematic reviews. Int. J. Dent. Hyg. 2018; 6(4): 441–449. DOI: 10.1111/idh.12336
  34. DeRiso A.J. II, Ladowski J.S., Dillon T.A., et al. Chlorhexidine gluconate 0.12% oral rinse reduces the incidence of total nosocomial respiratory infection and nonprophylactic systemic antibiotic use in patients undergoing heart surgery. Chest. 1996; 109(06): 1556–1561.
  35. Gjermo P. Chlorhexidine in dental practice. J. Clin. Periodontol. 1974; 1(03): 143–152.
  36. Briner W.W., Grossman E., Buckner R.Y. Effect of chlorhexidine gluconate mouthrinse on plaque bacteria. J. Periodontal. Res. 1986; 21(Suppl. 16): 44–52.
  37. Chan E.Y., Ruest A., Meade M.O., Cook D.J. Oral decontamination for prevention of pneumonia in mechanically ventilated adults: systematic review and meta-analysis. BMJ 2007; 334(7599): 889.
  38. Labeau S.O., Van de Vyver K., Brusselaers N., et al. Prevention of ventilator-associated pneumonia with oral antiseptics: a systematic review and meta-analysis. Lancet Infect. Dis. 2011; 11(11): 845–854. DOI: 10.1016/S1473–3099(11)70127-X
  39. Hua F., Xie H., Worthington H.V., et al. Oral hygiene care for critically ill patients to prevent ventilator-associated pneumonia. Cochrane Database Syst Rev 2016; 10: CD008367.
  40. Coffin S.E., Klompas M., Classen D., et al. Strategies to prevent ventilator-associated pneumonia in acute care hospitals. Infect Control. Hosp. Epidemiol. 2008; 29(Suppl. 1): 31–40.
  41. Muscedere J., Dodek P., Keenan S., Fowler R., Cook D., Heyland D.; VAP Guidelines Committee and the Canadian Critical Care Trials Group. Comprehensive evidence-based clinical practice guidelines for ventilator-associated pneumonia: diagnosis and treatment. J. Crit. Care. 2008; 23(01): 138–147. DOI: 10.1016/j.jcrc.2007.12.008
  42. Klompas M. Oropharyngeal Decontamination with Antiseptics to Prevent Ventilator-Associated Pneumonia: Rethinking the Benefits of Chlorhexidine. Semin Respir Crit. Care Med. 2017; 38(3): 381–390. DOI: 10.1055/s-0037-1602584
  43. Klompas M., Speck K., Howell M.D., et al. Reappraisal of routine oral care with chlorhexidine gluconate for patients receiving mechanical ventilation: systematic review and meta-analysis. JAMA Intern. Med. 2014; 174(05): 751–761. DOI: 10.1001/jamainternmed.2014.359
  44. Price R., MacLennan G., Glen J.; SuDDICU Collaboration. Selective digestive or oropharyngeal decontamination and topical oropharyngeal chlorhexidine for prevention of death in general intensive care: systematic review and network meta-analysis. BMJ 2014; 348: g2197. DOI: 10.1136/bmj.g2197
  45. Klompas M., Li L., Kleinman K., et al. Associations between ventilator bundle components and outcomes. JAMA Intern. Med. 2016; 176(09): 1277–1283. DOI: 10.1001/jamainternmed.2016.2427
  46. Hirata K., Kurokawa A. Chlorhexidine gluconate ingestion resulting in fatal respiratory distress syndrome. Vet. Hum. Toxicol. 2002; 44(02): 89–91.
  47. Kempen P.M. A tale of silent aspiration: are guidelines good for every patient? Anesth. Analg. 2015; 121(03): 829–831. DOI: 10.1213/ANE.0000000000000852
  48. Orito K., Hashida M., Hirata K., et al. Effects of single intratracheal exposure to chlorhexidine gluconate on the rat lung. Drug. Chem. Toxicol. 2006; 29(01): 1–9.
  49. Xue Y., Zhang S., Yang Y., et al. Acute pulmonary toxic effects of chlorhexidine (CHX) following an intratracheal instillation in rats. Hum. Exp. Oxicol. 2011; 30(11): 1795–1803. DOI: 10.1177/0960327111400104
  50. Massano G., Ciocatto E., Rosabianca C., et al. Striking aminotransferase rise after chlorhexidine self-poisoning. Lancet. 1982; 1(8266): 289.
  51. Plantinga N.L., Wittekamp B.H., Leleu K., et al. Oral mucosal adverse events with chlorhexidine 2 % mouthwash in ICU. Intensive Care Med. 2016; 42(04): 620–621. DOI: 10.1007/s00134-016-4217-7
  52. Deschepper M., Waegeman W., Eeckloo K., et al. Effects of chlorhexidine gluconate oral care on hospital mortality: a hospital-wide, observational cohort study. Intensive Care Med. 2018; 44(7): 1017–1026. DOI: 10.1007/s00134-018-5171-3
  53. Klompas M. What is new in the prevention of nosocomial pneumonia in the ICU? Curr. Opin. Crit. Care. 2017; 5: 378–384. DOI: 10.1097/MCC.0000000000000443
  54. Wang L., Li X., Yang Z., et al. Semi-recumbent position versus supine position for the prevention of ventilator-associated pneumonia in adults requiring mechanical ventilation. Cochrane Database Syst. Rev. 2016; 1: CD009946. DOI: 10.1002/14651858.CD009946.pub2
  55. Li Bassi G., Panigada M., Ranzani O.T., et al. Multicenter randomized clinical trial of lateral-trendelenburg vs. semi recumbent position for the prevention of ventilator-associated pneumonia — the GRAVITY-VAP Trial. Intensive Care Med. 2017; 43(11): 1572–1584. DOI: 10.1007/s00134-017-4858-1
  56. Esteban A., Frutos F., Tobin M.J., et al. A comparison of four methods of weaning patients from mechanical ventilation. Spanish Lung Failure collaborative Group. N. Engl. J. Med. 1995; 332: 345–350.
  57. Ely E.W., Baker A.M., Dunagan D.P., et al. Effect on the duration of mechanical ventilation of identifying patients capable of breathing spontaneously. N. Engl. J. Med. 1996; 335: 1864–1869.
  58. Kress J.P., Pohlman A.S., O’Connor M.F., Hall J.B. Daily interruption of sedative infusions in critically ill patients undergoing mechanical ventilation. N. Engl. J. Med. 2000; 342: 1471–1477.
  59. Girard T.D., Kress J.P., Fuchs B.D., et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (awakening and breathing controlled trial): a randomised controlled trial. Lancet. 2008; 371: 126–134.
  60. Caroff D.A., Li L., Muscedere J., Klompas M. Subglottic secretion drainage and objective outcomes: a systematic review and meta-analysis. Crit. Care Med. 2016; 44: 830–840. DOI: 10.1097/CCM.0000000000001414
  61. Bo L., Li J., Tao T., et al. Probiotics for preventing ventilator-associated pneumonia. Cochrane Database Syst. Rev. 2014; 10: CD009066. DOI: 10.1002/14651858.CD009066.pub2
  62. Zeng J., Wang C.T., Zhang F.S., et al. Effect of probiotics on the incidence of ventilator-associated pneumonia in critically ill patients: a randomized controlled multicenter trial. Intens Care Med. 2016; 42: 1018–1028. DOI: 10.1007/s00134-016-4303-x
  63. Cook D.J., Johnstone J., Marshall J.C., et al. Probiotics: prevention of severe pneumonia and endotracheal colonization trial-PROSPECT: a pilot trial. Trials. 2016; 17: 377. DOI: 10.1186/s13063-016-1495-x
  64. Weng H., Li J.G., Mao Z., Feng Y., et al. Probiotics for Preventing Ventilator-Associated Pneumonia in Mechanically Ventilated Patients: A Meta-Analysis with Trial Sequential Analysis. Front Pharmacol. 2017; 8: 717. DOI: 10.3389/fphar.2017.00717
  65. Bos L.D., Stips C., Schouten L.R., et al. Selective decontamination of the digestive tract halves the prevalence of ventilator-associated pneumonia compared to selective oral decontamination. Intensive Care Med. 2017; 43(10): 1535–1537. DOI: 10.1007/s00134-017-4838-5
  66. Daneman N., Sarwar S., Fowler R.A., et al. Effect of selective decontamination on antimicrobial resistance in intensive care units: a systematic review and meta-analysis. Lancet Infect. Dis. 2013; 13: 328–341. DOI: 10.1016/S1473–3099(12)70322–5
  67. Russell C.J., Shiroishi M.S., Siantz E., et al. The use of inhaled antibiotic therapy in the treatment of ventilator-associated pneumonia and tracheobronchitis: a systematic review. BMC Pulm. Med. 2016; 8; 16: 40. DOI: 10.1186/s12890-016-0202-8
  68. Póvoa F.C.C., Cardinal-Fernandez P., Maia I.S., et al. Effect of antibiotics administered via the respiratory tract in the prevention of ventilator-associated pneumonia: A systematic review and meta-analysis. J. Crit. Care. 2018; 43: 240–245. DOI: 10.1016/j.jcrc.2017.09.019

Respiratory mechanics and gas exchange during respiratory support in patients with necrotizing pancreatitis depending on the outcome

D.V. Gaigolnik1, K.Yu. Belyaev1, E.A. Gritsan2, A.I. Gritsan1,2

1 Krasnoyarsk Regional Clinical Hospital, Regional Public Health Institution, Krasnoyarsk

2 Krasnoyarsk State Medical University named after professor V.F. Voyno-Yasenetsky, Ministry of Health of the Russian Federation, Krasnoyarsk

For correspondence: Alexey I. Gritsan, Dr. Med. Sci., Professor, Chief of the Department of Anaesthesiology and Intensive Care Krasnoyarsk of the State Medical University named after Professor V.F. Voyno-Yasenetsky, Ministry of Health of the Russian Federation, Krasnoyarsk; e-mail: gritsan67@mail.ru

For citation: Gaigolnik DV, Belyaev KYu, Gritsan EA, Gritsan AI. Respiratory mechanics and gas exchange during respiratory support in patients with necrotizing pancreatitis depending on the outcome. Alexander Saltanov Intensive Care Herald. 2019;1:65–77.

DOI: 10.21320/1818-474X-2019-1-65-77


Objective. To compare the dynamics of ventilation parameters, mechanical properties of the lungs and gas exchange in the process of respiratory support in patients with a favorable and unfavorable outcome of intensive treatment of necrotic pancreatitis.

Methods. The work is based on the results of a single-center observational study. The results of treatment of 94 patients aged from 25 to 65 years with necrotic pancreatitis complicated by acute respiratory distress syndrome and sepsis are analyzed. All patients were divided into two groups: group 1 (68 patients with severe sepsis), group 2 (26 patients with severe sepsis complicated by septic shock). Within each group, patients were divided into two subgroups: the group of sepsis — patients with a favorable outcome (28 patients) and unfavorable outcome (40 patients), in the group of septic shock — patients with a favorable outcome (5 patients) and unfavorable outcome (21 patients). All patients were treated with complex therapy according to international and Russian guidelines for the treatment of pancreatic necrosis, sepsis, and acute respiratory distress syndrome. The evaluation of the mechanical properties of the lungs was performed in patients based on the parameters recorded in the IVL card: F, Vt, MV, PIP, PEEP, CPAP, Clt, Flow.

Dynamic assessment of gas exchange was carried out by continuous monitoring of SpO2, PetCO2, plethysmography and according to gas analysis. The data were recorded in the mechanical ventilation map with the subsequent calculation of some indicators: FiO2, PaO2, PaCO2, pH, AaDO2, PaO2/FiO2.

Results. Patients with necrotizing pancreatitis with a favorable outcome in the process of artificial ventilation of the lungs to ensure sufficient oxygenation during septic shock use significantly higher (by 16.0–18.3 %) levels of PIP and PEEP than in sepsis, as well as more significant disorders of gas exchange in the lungs (by AaDO2 and PaO2/FiO2) compared with sepsis. In sepsis and septic shock with an unfavorable outcome (in comparison with a favorable one), during respiratory support, more pronounced disorders of oxygen status are observed, which indicates the presence of a more severe acute respiratory distress syndrome. In sepsis with a favorable outcome, as opposed to unfavorable, there is a direct correlation between positive changes in oxygen status (PaO2/FiO2) and Vt, PIP, PEEP levels, whereas in septic shock there is no such relationship.

Conclusion. The obtained results allowed us to offer a starting regimen of respiratory support for ARDS in patients with necrotic pancreatitis.

Keywords: necrotic pancreatitis, sepsis, acute respiratory distress syndrome, respiratory support, respiratory biomechanics, gas exchange

Received: 05.11.2018


References

  1. Greer S.E., Burchard K.W. Acute pancreatitis and critical illness: a pancreatic tale of hypoperfusion and inflammation. Chest. 2009; 136 5): 1413–1419. DOI: 10.1378/chest.08-2616
  2. Johnson C.D., Besselink M.G., Carter R. Acute pancreatitis. BMJ. 2014; 349: g4859. DOI: 10.1136/bmj.g4859
  3. Pierrakos C. The changing pattern of acute respiratory distress syndrome over time: a comparison of two periods. C. Pierrakos, J.L. Vincent. Eur. Respir. J. 2012; 40(3): 589–595. DOI: 10.1183/09031936.00130511
  4. Chen Q., De-chao L.V., Bin C.A.O., et al. Study on risk factors of severe pancreatitis complicated with lung injury [Electronic resource]. J. Hepatopancr. Surg. 2012; 6. URL: http://en.cnki.com.cn/Article_en/CJFDTotal-GDYW201206005.htm
  5. Wolff C.B. Oxygen delivery: the principal role of the circulation. Adv. Exp. Med. Biol. 2013; 789: 37–42. DOI: 10.1007/978-1-4614-7411-1_6
  6. Shields C.J., Winter D.C., Redmond H.P. Lung injury in acute pancreatitis: mechanisms, prevention, and therapy. Curr. Opin. Crit. Care. 2002; 8(2): 158–163. DOI:10.4172/2165–7092.1000e149
  7. Elder A.S., Saccone G.T., Dixon D.L. Dixon injury in acute pancreatitis: mechanisms underlying augmented secondary injury. Pancreatology. 2012; 12(1): 49–56.
  8. Lundberg A.H., Granger D.N., Russell J., et al. Quantitative measurement of P- and E-selectin adhesion molecules in acute pancreatitis: correlation with distant organ injury. Ann. Surg. 2000; 231(2): 213–222.
  9. Власенко А.В. Дифференциальная диагностика и лечение вариантов острого респираторного дистресс-синдрома: автореф. дис. … д-ра мед. наук: 14.01.20. М., 2012.
  10. [Vlasenko A.V. Differential diagnosis and treatment of variants of acute respiratory distress syndrome: Author. dis. … Dr. med Sciences: 14.01.20. M., 2012. (In Russ)]
  11. Мороз В.В., Голубев А.М. Классификация острого респираторного дистресс-синдрома. Общая реаниматология. 2007; 3(5–6): 7–9. [Moroz V.V., Golubev A.M. Classification of acute respiratory distress syndrome. General reanimatology. 2007; 3(5–6): 7–9. (In Russ)]
  12. Pezzilli R., Bellacosa L., Felicani C. Lung injury in acute pancreatitis. JOP. 2009; 10(5): 481–484.
  13. Кассиль В.Л., Сапичева Ю.Ю, Хапий Х.Х. Острый респираторный дистресс-синдром и гипоксемия. М: МЕДпресс-информ, 2014.
  14. [Kassil V.L., Sapicheva Yu.Y., Hapiy Kh.Kh. Acute respiratory distress syndrome and hypoxemia. M: MEDpress-inform, 2014. (In Russ)]
  15. Багненко С.Ф., Шах Б.Н., Лапшин В.Н. и др. Коррекция расстройств микроциркуляции и профилактика реперфузионных нарушений у пострадавших с сочетанной шокогенной травмой. Клин. физиология кровообращения. 2007; 4: 49–55.
  16. [Bagnenko S.F., Shah B.N., Lapshin V.N. Correction of microcirculation disorders and prevention of reperfusion disorders in victims with combined shock injury. Clinical Physiology of Circulation. 2007; 4: 49–55. (In Russ)]
  17. Raghu M.G., Wig J. D., Kochhar R. et al. Lung complications in acute pancreatitis. JOP. 2007; 8(2): 177–185.
  18. Esteban A., Alia I., Gordo F. Prospective randomized trial comparing pressure-controlled ventilation and volume-controlled ventilation in ARDS. For the Spanish Lung Failure Collaborative Group. Chest. 2000; 117(6): 1690–1696. DOI.org/10.1378/chest.117.6.1690
  19. Bernard G.R., et al. Report of the American — European Consensus Conference on Acute Respiratory Distress Syndrome: Definitions, mechanisms, relevant outcomes, and clinical trial coordination. J. Crit. Care. 1994; 9: 72–81.
  20. Ranieri V.M., Rubenfeld G.D., Thompson B.T., et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012; 307(23): 2526–2533. DOI: 10.1001/jama.2012.5669
  21. The Third International Consensus definitions for sepsis and septic shock (Sepsis-3). Singer M., et al. JAMA. 2016; 315(8): 801–810. DOI:10.1001/jama.2016.0287
  22. Агаев Б.А., Джафарли З.Е. Комплексное лечение острого панкреатита/ Хирургия. Журн. им. Н.И. Пирогова. 2010; 4: 63–66.
  23. [Agaev B.A., Jafarli Z.E. Comprehensive treatment of acute pancreatitis. Surgery. Journal named N.I. Pirogov. 2010; 4: 63–66. (In Russ)]
  24. Деструктивный панкреатит. Доказательные методы диагностики и лечения. Под ред. В.С. Савельева. М.: РАСХИ, 2010: 12. [Destructive pancreatitis. Evidence-based diagnostic and treatment methods. ed. Saveliev V.S. M.: RASHI, 2010: 12. (In Russ)]
  25. Вычужанин Д.В., Егоров А.В., Левкин В.В. и др. Диагностика и профилактика послеоперационного панкреатита. Хирургия. Журн. им. Н.И. Пирогова. 2012; 4: 63–69.                [Vychuzhanin D.V., Egorov A.V., Levkin V.V., et al. Diagnosis and prevention of postoperative pancreatitis.Surgery. Journal named N.I. Pirogov. 2012; 4: 63–69. (In Russ)]
  26. Стяжкина С.Н., Ситников В.А., Леднева А.В. и др. Острый деструктивный панкреатит: диагностика и лечение. Междунар. журн. приклад. и фунд. исслед. 2011; 5: 110–112.
  27. [Styazhkina S.N., Sitnikov V.A., Ledneva A.V., et al. Acute destructive pancreatitis: diagnosis and treatment. International Journal of Applied and Fundamental Research. 2011; 5: 110–112. (In Russ)]
  28. Самигулина Г.Р., Спиридонова Е.А., Ройтман Е.В. и др. Острый деструктивный панкреатит: этиология, классификация, особенности течения. Вестн. интенсив. терапии. 2012; 4: 10–13.             [Samigulina G.R., Spiridonova E.A., Roitman E.V., et al. Acute destructive pancreatitis: etiology, classification, particularities of the course. Vestnik intensive therapy. 2012; 4: 10–13. (In Russ)]
  29. Dellinger R.P., Levy M.M., Rhodes A., et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit. Care Med. 2013; 41(2): 580–637. DOI: 10.1097/CCM.0b013e31827e83af
  30. Грицан А.И., Колесниченко А.П., Власенко А.В. и др. Диагностика и интенсивная терапия острого повреждения легких и острого респираторного дистресс-синдрома. Сборник материалов III Международного конгресса по респираторной поддержке. Красноярск. 2009.   [Gritsan A.I., Kolesnichenko A.P., Vlasenko A.V. et al. Diagnosis and intensive care for acute lung injury and acute respiratory distress syndrome. Collection of materials of the III International Congress on respiratory support, Krasnoyarsk. 2009. (In Russ)]
  31. Грицан А.И., Ярошецкий А.И., Власенко А.В. и др. Диагностика и интенсивная терапия острого респираторного дистресс-синдрома. Клинические рекомендации ФАР. Анестезиология и реаниматология. 2016; 61(1): 62–70. DOI: 10.18821/0201-7563-2016-61-1-62-70
  32. [Gritsan A.I., Yaroshetzkiy A.I., Vlasenko A.V. et al. Diagnostics and intensive therapy of acute respiratory distress syndrome. FARʼs clinical guidelines. 2016; 61(1): 62–70. DOI: 10.18821/0201-7563-2016-61-1-62-70. (In Russ)]
  33. Chiumello D., Marino A., Brioni M., et al. Visual anatomical lung CT scan assessment of lung recruitability. Intensive Care Med. 2013; 39(1): 66–73. DOI: 10.1007/s00134-012-2707-9
  34. Suzumura E.A., Amato M.B.P., Cavalcanti A.B. Understanding recruitment maneuvers. Intensive Care Med. 2016; 42(5): 908–911. DOI: 10.1007/s00134-015-4025-5
  35. Murray J.F., Matthay M.A., Luce J.M., et al. An expanded definition of the adult respiratory distress syndrome. Am. Rev. Respir. Dis. 1988; 138: 720–723; erratum 1989; 139: 1065.

Clinical predictors of neonatal sepsis

R.Kh. Gizatullin, P.I. Mironov

Bashkir State Medical University, Ufa, Russian Federation

For correspondence: Mironov Petr Ivanovich — Dr. Med. Sci., professor of the department of anesthesiology Bashkir State Medical University, Ufa; e-mail: mironovpi@mail.ru

For citation: Gizatullin R.Kh., Mironov P.I. Clinical predictors of neonatal sepsis. Alexander Saltanov Intensive Care Herald. 2018;4:38–41.

DOI: 10.21320/1818-474X-2018-4-38-41


One of the key issues in the fight against sepsis is the early detection of its predictors. The aim of the work is to identify predictors the development of neonatal sepsis.

Methods. Design-retrospective, observational, single-center. The development included 163 newborns with sepsis, 34 died. The Kulbak measure was used to assess the informativeness of the studied clinical and laboratory variables. The function of response was taken as the outcome of the disease: survived or died.

Results. The analysis of the informative value of clinical and laboratory parameters in newborns on the risk of development of lethal outcome.

Conclusion. The predictors of early neonatal sepsis include indicators of the number of blood platelets, total blood protein, body weight and the number of blood neutrophils. Their critical threshold values are also calculated.

Keywords: sepsis, newborns, early predictors

Received: 29.08.2018


References

  1. Goldstein B., Giroir B., Randolph A., et al. International pediatric sepsis consensus conference: Definitions for sepsis and organ dysfunction in pediatrics. Pediatr. Crit. Care Med. 2005; 6(1): 2–8. DOI: 10.1097/01.PCC.0000149131.72248.E6.
  2. Scott H.F., Deakyne S.J., Woods J.M., Bajaj L. The prevalence and diagnostic utility of systemic inflammatory response syndrome vital signs in a pediatric emergency department. Acad. Emerg. Med. 2015; 22: 381–389. DOI: 10.1111/acem.12610.
  3. Singer M., Deutschman C.S., Seymour C.W., et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016; 315(8): 801–810. DOI: 10.1001/jama.2016.0287.
  4. Schlapbach L.J., Straney L., Bellomo R., MacLaren G., Pilcher D. Prognostic accuracy of age-adapted SOFA, SIRS, PELOD-2, and qSOFA for in-hospital mortality among children with suspected infection admitted to the intensive care unit. Intensive Care Med. 2018; 44(2): 179–188. DOI: 10.1007/s00134-017-5021-8.
  5. Cheryl P., Srinivas M., Rollin B., et al. Mortality Risk Using a Pediatric Quick Sequential (Sepsis-Related) Organ Failure Assessment Varies With Vital Sign Thresholds. Pediatric Critical Care Medicine. 2018; 19(8): e394–e402. DOI: 10.1097/PCC.0000000000001598.
  6. ИвановД.О., Шабалов Н.П., Петренко Ю.В. Неонатальный сепсис. Опыт построения гипотезы. Детская медицина Северо-Запада. 2012; 3: 37–45. [Ivanov D.O., Shabalov N.P., Petrenko Ju.V. Neonatalʼnyj sepsis. Opyt postroenija gipotezy. Detskaja medicina Severo-Zapada. 2012; 3: 37–45. (In Russ)]
  7. ГолубцоваЮ.М., Дегтярев Д.Н. Современные подходы к профилактике, диагностике и лечению раннего неонатального сепсиса. Неонатология. 2014; 2: 15–26. [Golubcova Ju.M., Degtjarev D.N. Sovremennye podhody k prfilaktike, diagnostike i lecheniju rannego neonatalʼnogo sepsisa. Neonatologija. 2014; 2: 15–26. (In Russ)]
  8. КульбакС. Теория информативности и статистика. М.: Наука, 1967. [Kulʼbak S. Teorija informativnosti i statistika. M.: Nauka, 1967. (In Russ)]
  9. Weiss S.L., Deutschman C.S. Are septic children really just “septic little adults”? Intensive Care Med. 2018; 44: 392–394. DOI:10.1007/s00134-017-5007-6.

 

LPS-adsorber in patients with septic shock

S.P. Loginov1, E.G. Gromova2, M.V. Kiselevskij2, N.P. Krotenko1, Ju.I. Doljikova2, R.Ja. Vlasenko2, L.S. Kuznetsova2

1 Botkinskaia State Hospital, Moscow

2 Federal State Budgetary Institution “N.N. Blokhin National Medical Research Center of Oncology” of the Ministry of Health of the Russian Federation, Moscow

For correspondence: Gromova Elena Georgievna — MD, Head of the Intensive Care Unit № 2 FBSI “N.N. Blokhin NMRCO”, Moscow; e-mail: e_gromova05@mail.ru

For citation: Loginov SP, Gromova EG, Kiselevskij MV, Krotenko NP, Doljikova JuI, Vlasenko RJa, Kuznetsova LS. LPS-adsorber in patients with septic shock. Alexander Saltanov Intensive Care Herald. 2018;3:46–52.

DOI: 10.21320/1818-474X-2018-3-46-52


The results of lipopolysaccharide (LPS) sorption using selective LPS adsorber (Alteco) in 20 patients with gram-negative sepsis were investigated. From 2 to 6 hemoperfusion operations were performed. Concentrations of interleukins (IL): IL-6, IL-8, IL-10, IL-18, lipopolysaccharide (LPS) in serum before and after the procedure, and in washouts from sorbents were controlled. Decrease in LPS was accompanied by improvement or normalization of clinical and laboratory parameters, more pronounced in the group of survivors. High sorption capacity of LPS-adsorber and its efficiency in elimination of not only LPS but cytokine excess from the blood flow have been demonstrated.

Keywords: sepsis, septic shock, Alteco LPS adsorber, LPS, interleukins

Received: 07.08.2018


References

  1. Kaukonen K.M., Bailey M., Suzuki S., et al. Mortality related to severe sepsis and septic shock among critically ill patients in Australia and New Zealand, 2000–2012. JAMA. 2014; 311(13): 1308–1316.
  2. Анисимова Н.Ю., Громова Е.Г., Кузнецова Л.С. и др. Динамика элиминации бактериальных эндотоксинов и цитокинов из крови онкологических больных с сепсисом при гемосорбции с использованием угольных сорбентов. Бюллетень экспериментальной биологии и медицины. 2011; 151(5): 560–562. [Anisimova N.Yu., Gromova E.G., Kuznetsova L.S., et al. Dinamika eliminacii bakterialʼnyh endotoksinov i citokinov iz krovi onkologicheskih bolʼnyh s sepsisom pri gemosorbcii s ispolʼzovaniem ugolʼnyh sorbentov. Byulletenʼ eksperimentalʼnoj biologii i mediciny. 2011; 151(5): 560–562. (In Russ)]
  3. Анисимова Н.Ю., Киселевский М.В., Громова Е.Г., Кузнецова Л.С. Селективная и неселективная гемосорбция в интенсивной терапии онкологических больных с тяжелым сепсисом. Медицинский алфавит. 2011; 4(18): 29–33. [Anisimova N.Yu., Kiselevskij M.V., Gromova E.G., Kuznetsova L.S. Selektivnaya i neselektivnaya gemosorbciya v intensivnoj terapii onkologicheskih bolʼnyh s tyazhyolym sepsisom. Medicinskij alfavit. 2011; 4(18): 29–33. (In Russ)]
  4. Angus D.C., Linde-Zwirble W.T., Lidicker J., et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit. Care Med. 2001; 29(7): 1303–1310.
  5. Cinel I., Opal S.M. Molecular biology of inflammation and sepsis: a primer. Crit. Care Med. 2009; 37(1): 291–304.
  6. Kulabukhov V.V. Use of an endotoxin adsorber in the treatment of severe abdominal sepsis. Acta Anaesthesiol. Scand. 2008; 52(7): 1024–1025.
  7. Ronco C., d’Intini V., Bellomo R., et al. Обоснование применения экстракорпоральных методов лечения при сепсисе. Анестезиология и реаниматология. 2005; 2: 87–91. [Ronco C., d’Intini V., Bellomo R., et al. Obosnovanie primeneniya ekstrakorporalʼnyh metodov lecheniya pri sepsise. Anesteziologiya i reanimatologiya. 2005; 2: 87–91. (In Russ)]
  8. Ярустовский М.Б., Абрамян М.В., Попок З.В., и др. Селективная гемоперфузия при грамотрицательном тяжелом сепсисе у больных после кардиохирургических операций: проспективное рандомизированное исследование. Анестезиология и реаниматология. 2010; 6: 60–65. [Yarustovskij M.B., Abramyan M.V., Popok Z.V., et al. Selektivnaya gemoperfuziya pri gramotricatelʼnom tyazhelom sepsise u bolʼnyh posle kardiohirurgicheskih operacij: prospektivnoe randomizirovannoe issledovanie. Anesteziologiya i reanimatologiya. 2010; 6: 60–65. (In Russ)]
  9. Yaroustovsky M., Abramyan M., Popok Z., et al. Preliminary Report regarding the Use of Selective Sorbents in Complex Cardiac Surgery Patients with Extensive Sepsis and Prolonged Intensive Care Stay. Blood Purif. 2009; 28(3): 227–233.
  10. Blomquist S., Gustafsson V., Manolopoulos T., Pierre L. Clinical experience with a novel endotoxin adsorbtion device in patients undergoing cardiac surgery. Perfusion. 2009; 24(1): 13–17.
  11. Ala-Kokko T.I., Laurila J., Koskenkari J. A New Endotoxin Adsorber in Septic Shock: Observational Case Series. Blood Purif. 2011; 32(4): 303–309.
  12. Shum H.P., Leung Y.W., Lam S.M., et al. Alteco endotoxin hemoadsorption in Gram-negative septic shock patients. Indian J. Crit. Care Med. 2014; 18(12): 783–788.
  13. Lipcsey M., Tenhunen J., Sjölin J., et al. Abdominal Septic Shock — Endotoxin Adsorption Treatment (ASSET) — endotoxin removal in abdominal and urogenital septic shock with the Alteco® LPS Adsorber: study protocol for a double-blinded, randomized placebo-controlled trial. Trials. 2016; 17(1): 587–597.
  14. Маевская М.В., Буеверов А.О. Цитокины в патогенезе алкогольного гепатита и возможности терапии. Российский журнал гастроэнтерологии, гепатологии, колопроктологии. 2009; 2: 14–19. [Maevskaya M.V., Bueverov A.O. Citokiny v patogeneze alkogolʼnogo gepatita i vozmozhnosti terapii. Rossijskij zhurnal gastroenterologii, gepatologii, koloproktologii. 2009; 2:14–19. (In Russ)]
  15. Zhou M., Cheng S., Yu J., Lu Q. Interleukin-8 for Diagnosis of Neonatal Sepsis: A Meta-Analysis. PLoS One. 2015; 10(5): e0127170.
  16. Колесниченко А.П., Мосякин Н.А., Распопин Ю.С., и др. Биомаркеры и эфферентные методы терапии тяжелого сепсиса. Вестник интенсивной терапии. 2015; 4: 11–15. [Kolesnichenko A.P., Mosyakin N.A., Raspopin Yu.S., et al. Biomarkyory i efferentnye metody terapii tyazhyologo sepsisa. Vestnik intensivnoj terapii. 2015; 4: 11–15. (In Russ)]
  17. Zhou F., Peng Z., Murugan R., Kellum J.A. Blood purification and mortality in sepsis: a meta-analysis of randomized trials. Crit. Care Med. 2013; 41(9): 2209–2220.
  18. Хорошилов С.Е., Карпун Н.А., Половников С.Г. и др. Селективная гемосорбция эндотоксина в лечении абдоминального сепсиса. Общая реаниматология. 2009; 5(6): 83. [Horoshilov S.E., Karpun N.A., Polovnikov S.G., et al. Selektivnaya gemosorbciya ehndotoksina v lechenii abdominal’nogo sepsisa. Obshchaya reanimatologiya. 2009; 5(6): 83. (In Russ)]
  19. Teichholz L.E., Kreulen Т., Herman M.V. et al. Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence of absence of asynergy. Am. J. Cardiol. 1976; 37(1): 7–11.
  20. Tuguz A.R., Kiselevsky M.V., Gromova E.G., Matveev V.B. Cytokines dynamics in the blood, urine and drainage liquid in the earlier postoperative period of kidney cancer patients. 18th UICC International Cancer Congress 30 June — 5 July, 2002. Oslo, Norway. P. 876.
  21. Surviving Sepsis Campaign. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Critical Care Med. 2013; 41(2): 580–637.
  22. Тугуз А.Р. Иммунопатогенез ранних послеоперационных осложнений у онкологических больных. Дисс. … докт. мед. наук. М., 2002. [Tuguz A.R. Immunopatogenez rannih posleoperacionnyh oslozhnenij u onkologicheskih bolʼnyh. Diss. … dokt. med. nauk. M., 2002. (In Russ)]
  23. Anisimova N.Yu. Immunological Pathogenesis of Sepsis and Use of Hemosorption for Treatment of Cancer Patients With Sepsis. Nova Science Publishers Inc., 2014: 75–115.

Selective Sorption of Endotoxin in Combined Therapy of Post-Traumatic Abdominal Sepsis

R.R. Zaitsev, A.Yu. Yakovlev, A.V. Abramov, D.V. Ryabikov, S.I. Chistyakov, Y.V. Il’in

Nizhny Novgorod Regional Clinical Hospital named after Semashko, Nizhny Novgorod

For correspondence: Aleksey Yurevich Yakovlev — doctor of medical sciences, Nizhny Novgorod Regional Clinical Hospital named after Semashko, Nizhny Novgorod; e-mail: aritnnru@list.ru

For citation: Zaitsev RR, Yakovlev AYu, Abramov AV, Ryabikov DV, Chistyakov SI, Il’in YV. Selective Sorption of Endotoxin in Combined Therapy of Post-Traumatic Abdominal Sepsis. Intensive Care Herald. 2017;2:21–25.


The investigations of the dynamics of lipopolysaccharide and presepsin in patients with closed abdominal trauma in the early post- traumatic period and after the development of abdominal sepsis. It revealed a biphasic rise of sepsis markers on stage fill hypovolemia and sepsis during subsequent development. High-performance determined early consistent application of selective sorption of LPS using «LPS adsorber» (Alteco, Sweden) and prolonged veno-venous hemofiltration in relation to the relief of endotoxemia and prevent the progression of multiple organ failure at post-traumatic abdominal sepsis.

Keywords: abdominal trauma, sepsis, LPS adsorber, hemofiltration, lipopolysaccharide, presepsin

Received: 10.03.2017


References

  1. Сепсис: классификация, клинико-диагностическая концепция и лечение: практич. руководство: Под ред. В.С. Савельева, Б.Р. Гельфанда. 2-е изд., доп. и перераб. М.: МИА, 2013. [Sepsis: klassifikatsiya, kliniko-diagnosticheskaya kontseptsiya i lechenie: praktich. rukovodstvo. Eds.: V.S. Savel’ev, B.R. Gel’fand. 2th Moscow: MIA, 2013. (In Russ)]
  2. Арискина О.Б., Пивоварова Л.П., Осипова И.В. и др. Влияние травматического токсикоза на иммунную реактивность пострадавших с шокогенной травмой. В сб.: Актуальные вопросы сочетанной шокогенной травмы и скорой помощи: Cб. науч. трудов, посвященный 70-летию НИИ скорой помощи им. И.И. Джанелидзе. СПб., 2002: 247–257. [Ariskina O.B., Pivovarova P., Osipova I.V. et al. Vliyanie travmaticheskogo toksikoza na immunnuyu reaktivnost’ postradavshih s shokogennoy travmoi. In: Aktual’nye voprosy sochetannoj shokogennoj travmy i skoroj pomoshchi: sbornik nauchnyh trudov, posvyashchennyj 70-letiyu NII skoroj pomoshchi im. I.I. Dzhanelidze. St.-Petersburg, 2002: 247–257. (In Russ)]
  3. Батюк В.И. Повышение резистентности организма к травматическому шоку. Новости хирургии. 2007; 1: 14–19. [Batyuk I. Povyshenie rezistentnosti organizma k travmatich- eskomu shoku. Novosti hirurgii. 2007; 1: 14–19. (In Russ)]
  4. Биленко М.В. Ишемические и реперфузионные повреждения органов (молекулярные механизмы, пути предупреждения и лечения). М.: Медицина, 1989. [Bilenko M.V. Ishemicheskie i reperfuzionnye povrezhdeniya organov (molekularnye mehanizmy, puti preduprezhdeniya i lecheniya). M.: Medicina, 1989. (In Russ)]
  5. Бондаренко В.М. Роль условно-патогенных бактерий кишечника в полиорганной патологии человека. М.: Триада, 2007. [Bondarenko M. Rol’ uslovno-patogennyh bakterii kishechnika v poliorgannoi patologii cheloveka. Moscow: Triada, 2007. (In Russ)]
  6. Вербицкая В.С. Влияние аргинина на функциональное состояние тонкой кишки в посттравматическом периоде ушиба сердца. Омский научный вестник. 2013; 1(118): 53–56. [Verbickaya V.S. Vliyanie arginina na funktsional’noe sostoyanie tonkoi kishki v posttravmaticheskom periode ushiba serdtsa. Omskij nauchnyj vestnik. 2013; 1(118): 53–56. (In Russ)]
  7. Еникеев Д.А., Нургалеева Е.А., Фаршатова Е.Р. и др. Влияние морфофункционального состояния брыжейки и кишечника в развитии эндотоксемии в постреанимационном периоде в эксперименте. Медицинский вестник Башкортостана. 2011; 6(1): 82–86. [Enikeev D.A., Nurgaleeva E.A., Far- shatova E.R. et al. Vliyanie morfofunktsional’nogo sostoyaniya bryzheiki i kishechnika v razvitii endotoksemii v postreanimat- sionnom periode v experimente. Medicinskij vestnik Bashkorto- stana. 2011; 6(1): 82–86. (In Russ)]
  8. Baxevanos N., Giamarellos-Bourboulis E.J., Pistiki A. et al. Bacterial translocation induces proinflammatory responses and is associated with early death in experimental severe J. Surg. Res. 2013; 185(2): 844–850. doi: 10.1016/j. jss.2013.07.026.
  9. Tanabe , Calland J.F., Schirmer B.D. Effects of peritoneal injury and endotoxin on myoelectric activity and transit. J. Surg. Res. 2004; 116(2): 330–336. doi: 10.1016/j.jss.2003.08.234.
  10. Zellweger R., Ayala A., Zhu X.L., Morrison M.H., Chaudry I.H. Effect of surgical trauma on splenocyte and peritoneal macrophage immune J. Trauma. 1995; 39(4): 645–650.
  11. Храмых Т.П., Долгих В.Т. К вопросу об эндотоксемии при геморрагической гипотензии. Патологическая физиология и экспериментальная терапия. 2009; 1: 28–30. [Hramyh T.P., Dolgih V.T. K voprosy ob endotoksemii pri gemorragicheskoi gipotenzii. Patologicheskaya fiziologiya i ehksperimental’naya terapiya. 2009; 1: 28–30. (In Russ)]
  12. Храмых Т.П., Долгих В.Т. Патогенез интоксикации при геморрагической гипотензии. Общая реаниматология. 2008; 5: 36–39. doi: 10.15360/1813-9779-2008-5-36. [Hramyh T.P., Dolgih V.T. Patogenez intoksikatsii pri gemorragicheskoi gipotenzii. Obshchaya reanimatologiya. 2008; 5: 36–39. doi: 10.15360/1813-9779-2008-5-36. (In Russ)]
  13. Chihara S., Masuda , Tatsumi H. et al. Early induction of direct hemoperfusion with a polymyxin_B immobilized column is associated with amelioration of hemodynamic derangement and mortality in patients with septic shock. J. Artif. Organs. 2016; 11: 23–37. doi: 10.1007/s10047-016-0922-9.
  14. Голубев А.М., Кузовлев А.Н., Сундуков Д.В., Голубев М.А. Морфологическая характеристика легких при ингаляции липополисахарида и перфторана. Общая реаниматология. 2015; 11(1): 6–13. doi: 10.15360/1813-9779-2015-1-6-13. [Golubev A.M., Kuzovlev A.N., Sundukov D.V., Golubev M.A. Morfo- logicheskaya harakteristika legkih pri ingalyatsii lipopolisaharida i perftorana. Obshchaya reanimatologiya. 2015; 11(1): 6–13. doi: 10.15360/1813-9779-2015-1-6-13. (In Russ)]
  15. Аниховская И.А., Кубатиев А.А., Майский И.А. и др. Направления поиска снижения концентрации эндотоксина в общей циркуляции. Патогенез. 2014; 12(4): 26–31. [Anihovskaya I.A., Kubatiev A.A., Majskij I.A. et al. Napravleniya poiska snizheniya kontsentratsii endotoksina v obshchei tsirkulyatsii. Patogenez. 2014; 12(4): 26–31. (In Russ)]
  16. Лиходед В.Г., Ющук Н.Д., Яковлев М.Ю. Роль эндотоксина грамотрицательных бактерий в инфекционной и неинфекционной патологи. Архив патологии. 1996; 2: 8–12. [Lihoded V.G., Yushchuk N.D., Yakovlev M.Yu. Rol’ endotoksina gramotritsatel’nyh bakterii v infektsionnoi i neinfektsionnoi pa- tologii. Arhiv patologii. 1996; 2: 8–12. (In Russ)]
  17. Ронко К., Пиччинни П., Рознер М.Г. Эндотоксемия и эндотоксический шок. Патогенез, диагностика и лечение. М.: Издатель И.В. Балабанов, [Ronko K., Pichchinni P., Rozner M.G. Endotoksemiya i endotoksicheskii shok. Patogenez, diagnostika i lechenie. M.: Izdatel’ I.V. Balabanov, 2012. (In Russ)]
  18. Яковлев М.Ю. Кишечный липополисахарид: системная эндотоксемия — эндотоксиновая агрессия — SIR-синдром и поли- органная недостаточность как звенья одной цепи. Бюллетень ВНЦ РАМН. 2005; 1: 15–18. [Yаkovlev M.Yu. Kishechnyi lipopolisaharid: sistemnaya endotoksemiya — endotoksinovaya agressiya — SIR-sindrom i poliorgannaya nedostatochnost’ kak zven’ya odnoi tsepi. Byulleten’ VNC RAMN. 2005; 1: 15–18. (In Russ)]

The First Experience of Cytokine Adsorption in the Patient with Sepsis after Cardiosurgical Procedure

D.L. Shukevich1, 2, G.P. Plotnikov1, M.S. Rubtsov1, V.G. Matveeva1, E.V. Grigoryev1, 2

1Scientific research institute for complex issues of cardiovascular diseases, Kemerovo

2Kemerovo State Medical University, Kemerovo

For correspondence: Grigoryev Evgeny — PhD, MD, Kemerovo; e-mail: grigev@kemcardio.ru

For citation: Shukevich DL, Plotnikov GP, Rubtsov MS, Matveeva VG, Grigoryev EV. The First Experience of Cytokine Adsorption in the Patient with Sepsis after Cardiosurgical Procedure. Intensive Care Herald. 2016;4:59–61.


Systemic inflammatory response is the basic for the host response against infectious and noninfectious agents. Cytokines are the leading mediators of the systemic inflammation. In patients with sepsis reduction of cytokines production may be useful to decrease the severity of the systemic inflammatory response and to ameliorate the multiorgan failure. We produce the case report — the successful experience of the intensive care of the septic patient after cardiac surgery with the help of cytokine adsorption. The normalization of hemodynamic status, the reduction of the SOFA scale and the decrease of the level of interleukin 6 confirmed the effectiveness of adsorption.

Keywords: systemic inflammatory response, sepsis, cytokine adsorption

Received: 07.10.2016


References

  1. Rimmelee T., Kellum J.A. Clinical review: blood purification for sepsis. Crit. Care. 2011; 15(1): 205. doi: 10.1186/cc9411.
  2. Cole L., Bellomo R., Journois D. et al. High-volume haemofiltration in human septic shock. Intensive Care Med. 2001; 27(6): 978–986. doi: 10.1007/s001340100963.
  3. Бердников А.П., Мусаева Т.С., Гончаренко С.И. Оценка эффективности комбинированного применения селективной липополисахаридной гемосорбции у больных с тяжелым сепсисом. Вестник интенсивной терапии. 2016; 5: 66–69. [Berdnikov A.P., Musaeva T.S., Goncharenko S.I. Evaluation of the effectiveness of the combined use of selective lipopolysaccharide hemosorption in patients with severe sepsis. Vestnik intensivnoy terapii. 2016; 5: 66–69. (In Russ)]
  4. Барбараш Л.С., Плотников Г.П., Шукевич Д.Л., Григорьев Е.В., Шукевич Л.Е. Гемодинамика и гидродинамический статус при системном воспалительном ответе инфекционной и неинфекционной этиологии на фоне продолжительной заместительной почечной терапии. Патология кровообращения и кардиохирургия. 2010; 4: 42–45. [Barbarash L.S., Plotnikov G.P., Shukevich D.L., Grigoryev E.V., Shukevich L.E. Hemodynamic and hydrodynamic status in the infectious and noninfectious systemic inflammatory response during continuous renal replacement therapy. Patologiya krovoobrascheniya i kardiohirurgiya. 2010; 4: 42–45. (In Russ)]
  5. Heering P., Morgera S., Schmitz F.J. et al. Cytokine removal and cardiovascular hemodynamics in septic patients with continuous venovenous hemofiltration. Intensive Care Med. 1997; 23(3): 288–296.
  6. Abraham E., Wunderink R., Silverman H. et al. Efficacy and safety of monoclonal antibody to human tumor necrosis factor alpha in patients with sepsis syndrome. A randomized, controlled, double-blind, multicenter clinical trial. TNF-alpha MAb Sepsis Study Group. 1995; 273(12): 934–941. doi: 10.1001/jama.1995.03520360048038.
  7. Peng Z.Y., Carter M.J., Kellum J.A. Effects of hemoadsorption on cytokine removal and short-term survival in septic rats. Crit. Care Med. 2008; 36(5): 1573–1577. doi: 10.1097/CCM.0b013e318170b9a7.
  8. Peng Z.Y., Wang H.Z., Carter M.J. et al. Acute removal of common sepsis mediators does not explain the effects of extracorporeal blood purification in experimental sepsis. Kidney Int. 2012; 81(4): 363–369. doi:1038/ki.2011.320.
  9. Hetz H., Berger R., Recknagel P., Steltzer H. Septic shock secondary to b-hemolytic streptococcus-induced necrotizing fasciitis treated with a novel cytokine adsorption therapy. Int. J. Artif. Organs. 2014; 37(5): 422–426. doi: 10.5301/ijao.5000315.
  10. Trager K., Fritzler D., Fischer G. et al. Treatment of post-cardiopulmonary bypass SIRS by hemoadsorption: a case series. Int. J. Artif. Organs. 2016; 39(3): 141–146. doi: 10.5301/ijao.5000492.
  11. Tomescu D.R., Olimpia Dima S., Ungureanu D. et al. First report of cytokine removal using CytoSorb in severe non-infectious inflammatory syndrome after liver transplantation. Int. J. Artif. Organs. 2016; 39(3): 136–140. doi: 10.5301/ijao.5000489.
  12. Gehling M., Tryba M. Is the time ripe for CytoSorb? Dtsch. Med. Wochenschr. 2016; 141(6): 428–429. doi: 10.1055/s-0041-110419.

Sepsis and liver dysfunction: state of the art (review)

S.P. Sviridova, Yu.I. Patyutko, A.V. Sotnikov

N.N. Blokhin Cancer Research Center, The Ministry of Healthcare of Russian Federation, Moscow, Russia

For citation: Sviridova SP, Patyutko YuI, Sotnikov AV. Sepsis and liver dysfunction: state of the art (review). Intensive Care Herald. 2016;1:3–12.


Cellular and molecular mechanisms of liver injury in sepsis are described. The liver plays a major role in a wide range of metabolic, homeostatic and defensive reactions in sepsis: the binding of bacteria and production of inflammatory mediators, as well as immuno-modulation. Numerous studies showed that oxidative stress and cytokine/endotoxin-mediated damage are the main pathogenetic mechanisms of liver injury in sepsis. Novel translational researches of the molecular mechanisms of severe sepsis conducted by authors from Austria, Germany and the UK provide a valuable view on the pathogenesis of liver dysfunction during sepsis. Shifts of plasma concentrations of bile acids in the early hours of sepsis are associated with liver dysfunction with high sensitivity and specificity, and clinical outcomes are associated with the severity of these changes and correlate with prognosis. Metabolic shifts and inflammatory reaction reduce biological transformation in the liver (especially activity of cytochrome P450 is decreased), resulting in significant deterioration of endo- and xeno-biotisc excretion. It was established that sepsis induces the reprogramming of metabolic liver functions in accordance with the severity of phase I and phase II biotransformation and tubular transport disorders. Inflammatory cytokines produced by the Kupffer cells lead to hepatocytes’ suppression of various ATP-dependent transporters involved in bile current resulting in intralobular cholestasis. Liver dysfunction plays role in many pathological processes and causes serious damage to metabolic state, immune response, coagulation, detoxification and antimicrobial protection. A better understanding of the liver pathophysiology in sepsis, early detection of liver dysfunction and prompt appropriate treatment of severe sepsis are crucial for improving of the survival rates.

Keywords: sepsis, systemic dysfunction, liver failure, liver dysfunction, cytokines.


References

  1. Hall M.J., Williams S.N., DeFrances C.J. et al. Inpatient care for septicemia or sepsis: a challenge for patients and hospitals. NCHS Data Brief 2011 Jun; (62):1-8.
  2. Mangia C.M., Kissoon N., Branchini O.A., et al. Bacterial sepsis in Brazilian children: a trend analysis from 1992 to 2006. PLoS One. 2011; 6(6): e14817. doi: 10.1371 / journal.pone.0014817.
  3. Vincent J.L., Taccone F., Schmit X. Classification, incidence, and outcomes of sepsis and multiple organ failure. Contrib Nephrol 2007;156:64-74.
  4. Angus D.C., van der Poll T. Severe sepsis and septic shock. N Engl J.Med 2013;369:840-51.
  5. Blanco J., Muriel-Bombín A., Sagredo V., et al. Incidence, organ dysfunction and mortality in severe sepsis: a Spanish multicentre study. Crit Care 2008, 12:R158.
  6. Gajewska K., Schroeder M., de Marre F., Vincent J.L. (2004). Analysis of terminal events in 109 successive deaths in a Belgian intensive care unit. Intensive Care Med 30:1224-1227.
  7. Marshall J. C. Measuring organ dysfunction in the intensive care unit. Why and how? Can. J. Anesth. 2005; 52 (3): 224-230.
  8. Engel C., Brunkhorst F.M., Bone H.G., et al. Epidemiology of sepsis in Germany: results from a national prospective multicenter study. Intensive Care Med. 2007; 33:606-18.
  9. Vishal Bansal, Jay Doucet. Multiple organ disfunction syndrome. Scientific American Surgery 06/2015 Critical Care 2015 Decker Intellectual Properties DOI 10.2310/7800.2160.
  10. Strassburg CP: Gastrointestinal disorders of the critically ill. Shock liver. Best Pract Res Clin Gastroenterol 17: 369-381, 2003.
  11. Bonde P., Ku N.C., Genovese E.A. Bermudez C.A. et al. Model and end-stage liver disease score predicts adverse events ralated to ventricular assist therapy. Ann Thorac Surg. 2012; 93:1541-7 discussion 1547-8.
  12. Nesseler N., Launey Y., Aninat C., et al. Clinical review: The liver in sepsis Critical Care 2012, 16:235 doi:10. 1186/cc11381.
  13. Horvatits T., Trauner M., Fuhrmann V. Hypoxic liver injury and cholestasis. Curr Opin Crit Care 2013, 19:128-132.
  14. Lescot Th., Karvellas C., Beaussier M., et al. Acquired Liver Injury in the Intensive Care Unit / Anesthesiology 10 2012, Vol.117, 898-904.
  15. Kramer L., Jordan B., Druml W., et al. Incidence and prognosis of early hepatic dysfunction in critically ill patients – a prospective multicenter study. Crit Care Med 2007; 35:1099-1104.
  16. Mesotten D., Wauters J., Van den Berghe G., et al. The effect of strict blood glucose control on biliary sludge and cholestasis in critically ill patients. J Clin Endocrinol Metab 2009; 94:2345-2352.
  17. Jäger B., Drolz A., Michl B.,. et al. Gaundice increases the rate of complications and one-year mortality in patients with hypoxic hepatitis. Hepatology. December 2012. Volume 56, Issue 6, pages 2297–2304. DOI:10.1002/hep.25896.
  18. Raurich J.M., Perez O., Llompart-Pou J.A., et al. Incidence and outcome of ischemic hepatitis complicating septic shock. Hepatol Res 2009; 39:700-705.
  19. Fuhrmann V., Kneidinger N., Herkner H., et al. Hypoxic hepatitis: underlying conditions and risk factors for mortality in critically ill patients. Intensive Care Med. 2009;35(8):1397-1405.
  20. Hawker F.: Liver dysfunction in critical illness. Anaesth Intensive Care 19:165-181, 1991.
  21. Geier A., Fickert P., Trauner M.: Mechanisms of disease: mechanisms and clinical implications of cholestasis in sepsis. Nat Clin Pract Gastroenterol Hepatol 2006. 3:574-585.
  22. Marshall J.C., Cook D.J., Christou N.V., et al. Multiple organ dysfunction score: A reliable descriptor of a complex clinical outcome. Crit Care Med (1995). 23: 1638-1652.
  23. Vincent J.L., Moreno R., Takala J., et al.: The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. Intensive Care Med 22:707-710, 1996.
  24. Hawker F.: Liver dysfunction in critical illness. Anaesth Intensive Care 1991; 19:165-181.
  25. Thomson S.J., Cowan M.L., Johnston I., et al.: «Liver function tests» on the intensive care unit: A prospective, observational study. Intensive Care Med 2009; 35:1406-11.
  26. Vanwijngaerden Y.M., Wauters J., Langouche L., et al. (2011) Critical illness evokes elevated circulating bile acids related to altered hepatic transporter and nuclear receptor expression. Hepatology 54: 1741-1752. doi: 10.1002/hep.24582.
  27. Kortgen A., Paxian M., Werth M., et al. Prospective assessment of hepatic function and mechanisms of dysfunction in the critically ill. Shock. 2009 Oct; 32(4):358-65. doi: 10.1097/SHK.0b013e31819d8204.
  28. Recknagel P., Gonnert F.A., Westermann M. et al.: Liver dysfunction and phosphatidylinositol-3-kinase signalling in early sepsis: experimental studies in rodent models of peritonitis. PLoS Med 2012, 9:e1001338. Jean-Louis Vincent, Academic Editor.
  29. Bauer M., Press A.T., Trauner M. The liver in sepsis: patterns of response and injury . Curr Opin Crit Care 2013, 19:123-127.
  30. Ивашкин В.Т. Механизмы иммунной толерантности и патологии печени // Российский журнал гастроэнтерологии, гепатологии, колопроктологии.- 2009. – N2 .- С. 2-13.
  31. McCuskey, R. S. The Hepatic Microvascular System in Health and Its Response to Toxicants / R. S. McCuskey //The anatomical record. – 2008. – N 291. – P. 661-671.
  32. Kmiec, Z. Cooperation of liver cells in health and disease /Z. Kmiec // Adv Anat Embryol Cell Biol.-2001. N 161, III-XIII, 1- P.151.
  33. Cheluvappa R, Denning GM, Lau GW, et al. Pathogenesis of the hyperlipidemia of Gram-negative bacterial sepsis may involve pathomorphological changes in liver sinusoidal endothelial cells. Int J Infect Dis 2010;14:e857-67.
  34. Glass C.K., Saijo K., (2010) Nuclear receptor transrepression pathways that regulate inflammation in macrophages and T cells. Nat. Rev. Immunol., 10(5): 365-376.
  35. Кайдашев И.П. NF-kB-сигнализация как основа развития системного воспаления, инсулинорезистентности, липотоксичности, сахарного диабета 2-го типа и атеросклероза// Междунар. эндокринол. журн., 2011.- №3(35).- С. 35–38.
  36. Park B.S., Song D.H., Kim H.M., et al. The structural basis of lipopolysaccharide recognition by the TLR4-MD-2 complex. // Nature. – 2009. – Vol. 458, № 7242. – P. 1191-1195.
  37. Medzhitov R., Janeway C. Innate immunity // The New England Journal of Medicine. 2000. – Vol. 8. – P. 338-344.
  38. Kawai T. et Akira S. TLR signaling // Semin. Immunol. 2007. -Vol. 19 (1). – P. 24-32.
  39. Parker L.C., Prince L.R., Sabroe I. Translational mini-review series on Toll-like receptors: networks regulated by Toll-like receptors mediate innate and adaptive immunity. Clin Exp Immunol. 2007; 147:199-207.
  40. Chawla A., Repa J.J., Evans R.M., et al. Nuclear receptors and lipid physiology: opening the X-files // Science. – 2001. – Vol. 294, № 5548. – P. 1866-1870.
  41. Francis G.A., Fayard E., Picard F., Auwerx J. Nuclear receptors and the control of metabolism. // Annu. Rev. Physiol. – 2003. – Vol. 65. – P. 261-311.
  42. Ивашкин В.Т. Ядерные рецепторы и патология печени. Часть 1-я.- РЖГГК, 2010.- №3, с.4-8.
  43. Расин М.С., Кайдашев И. П. Роль ядерных транскрипционных факторов в синтропии современной внутренней патологии (обзор литературы). Укр. Мед. Часопис. № 1 (99) – I/II 2014.- с. 17-21.
  44. Eipel Ch., Abshagen K., Vollmar B. Regulation of hepatic blood flow: The hepatic arterial buffer response revisited. World J Gastroenterol. 2010 Dec 28; 16(48): 6046-6057.
  45. Tamandl D., Jørgensen P., Gundersen Y., et al. Nitric oxide administration restores the hepatic artery buffer response during porcine endotoxemia. J Invest Surg 2008;21:183-94.
  46. Jakob S.M. Clinical review: Splanchnic ischaemia. Crit Care. 2002;6:306-312; 47. Dahn MS, Lange P, Lobdell K, et al. Splanchnic and total body oxygen consumption differences in septic and injured patients. Surgery 1987; 101:69-80.
  47. Fink M.P. Bench-to-bedside review: Cytopathic hypoxia // Critical Care. 2002. V. 6. P. 491-499.
  48. Takala J., Ruokonen E. Blood flow and oxygen transport in septic shock. // Clin. Intensive Care. 1992. Vol. 3. Р. 24-27.

(Полный список литературы находится в редакции – 135 источников).

Whether free hemoglobin can be a severity’s marker of general condition of the patient with sepsis?

Y.P. Orlov1, 3, V.T. Dolgikh2, A.V. Glushchenko3

1 The Department of Anesthesiology and Intensive Care, Federal state budgetary educational institution higher education “Omsk State Medical University” Ministry of Health of Russian Federation, Omsk

2 The Department of Pathophysiology with course of clinical pathophysiology, Federal state budget educational institution higher education “Omsk State Medical University” Ministry of Health of Russian Federation, Omsk

3 BUZOO “City clinical emergency hospital N 1», Omsk, Russia

For correspondence: Orlov Yuriy Petrovich — MD, Professor of Anesthesiology and reanimatology, Russian “Omsk State Medical University” the Ministry of health of Russia; e-mail: orlov-up@mail.ru

For citation: Orlov YP, Dolgikh VT, Glushchenko AV. Whether Free Hemoglobin can be a Severity’s Marker of General Condition of the Patient with Sepsis? Alexander Saltanov Intensive Care Herald. 2018;1:48–54.

DOI: 10.21320/1818-474X-2018-1-48-54


Purpose of Research: to determine whether we can use free hemoglobin concentration as early prognostic marker and a predictor of mortality in sepsis. Materials and Methods. In a retrospective study in 60 patients aged 47,6 ± 7,2 years with sepsis (30,4 ± 2,1 points on the Mannheim’s scale for evaluation of the severity of peritonitis) modern methods of statistics (ROC-analysis) hypothesis was tested, whether level of free hemoglobin in the first 24 hours from the moment of admission can be used as a biomarker for diagnosis and prognosis for severe sepsis. Informative criterion was compared with the information of the procalcitonin test. Results. The present study had shown that the above average free hemoglobin concentration, measured on the first day of the heavy flow of sepsis, is directly connected with increased 30-days mortality, and the level of free hemoglobin in a first day of the disease has high sensitivity, specificity, and can determine the outcome of sepsis with accuracy up to 96,7 %. Conclusion. Free hemoglobin concentration above medium size identified on the first day of the currents of severe sepsis, is directly related to increased 30-day mortality, and researched level of free hemoglobin in day 1 of the disease has a high proportion of sensitivity and specificity. Level of free hemoglobin is Predictor outcome of sepsis in the first 24 hours after the start of therapy, but the results did not rule out the need to use the necessary test from septic patients, but rather the feasibility of combining the two dictates the criteria to assess the outcome of severe septic process that requires further research.

Keywords: free hemoglobin, procalcitonin, sepsis, ROC-analysis

Received: 15.01.2018


References

  1. Weis S., Carlos A.R., Moita M.R., et al. Metabolic Adaptation Establishes Disease Tolerance to Sepsis. Cell. 2017; 169(7): 1263–1275. e14. doi: 10.1016/j.cell.2017.05.031.
  2. Harbarth S., Holeckova K., Froidevaux C., et al. Geneva Sepsis Network. Diagnostic value of procalcitonin, interleukin-6, and interleukin-8 in critically ill patients admitted with suspected sepsis. Am. J. Respir. Crit. Care Med. 2001; 164(3): 396–402.
  3. Selberg O., Hecker H., Martin M., et al. Discrimination of sepsis and systemic inflammatory response syndrome by determination of circulating plasma concentrations of procalcitonin, protein complement 3a, and interleukin-6. Crit. Care Med. 2000; 28(8): 2793–2798.
  4. Yu X., Ma X., Ai Y. Diagnostic value of serum procalcitonin for infection in the immunocompromised critically ill patients with suspected infection. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2015; 27(6): 477–483. doi: 10.3760/cma.j.issn.2095-4352.2015.06.012.
  5. Jordi Rello J., Francisco Valenzuela-Sánchez F., Ruiz-Rodriguez M., Moyano S. Sepsis: A Review of Advances in Management. Adv. Ther. 2017; 34(11): 2393–2411. doi: 10.1007/s12325-017-0622-8.
  6. Мчедлишвили Г.И. Гемореология в системе микроциркуляции: ее специфика и практическое значение. Тромбоз, гемостаз иреология. 2002; 4(12); 18–24. [Mchedlishvili G.I. Hemorheology in microcirculation system: its specificity and practical significance. Thrombosis, hemostasis and rheology. 2002; 4(12); 18–24. (In Russ)]
  7. Сторожук П.Г. Ферменты прямой и косвенной антирадикальной защиты эритроцитов и их роль в инициации процессов оксигенации гемоглобина, антибактериальной защите и делении клеток. Вестн. инт. терапии. 2000; 3: 8–13. [Storozhuk P.G. Enzymes direct and indirect antiradical protect red blood cells and their role in triggering processes of oxygenation of hemoglobin, antibacterial protection and cell division. Vestn. intensive therapy. 2000; 3: 8–13. (In Russ)]
  8. Huffman D.L., Bischof L.J., Griffitts J.S., Aroian R.V. Pore worms: using Caenorhabditis elegans to study how bacterial toxins interact with their target host. Int. J. Med. Microbiol. 2004; 293: 599–607. doi: 10.1078/1438-4221-00303.
  9. Aroian R., van der Goot F.G. Pore-forming toxins and cellular nonimmune defenses (CNIDs) Curr. Opin. Microbiol. 2007; 10: 57–61. doi: 10.1016/j.mib.2006.12.008.
  10. Gonzalez M.R., Bischofberger M., Pernot L., et al. Bacterial pore-forming toxins: the (w)hole story? Cell. Mol. Life Sci. 2008; 65: 493–507. doi: 10.1007/s00018-007-7434-y.
  11. Bull B.S., Kuhn I.N. The production of schistocytes by fibrin strands (a scanning electron microscope study). Blood. 1970; 35: 104–111.
  12. Heyes H., Köhle W., Slijepcevic B. The appearance of schistocytes in the peripheral blood in correlation to the degree of disseminated intravascular coagulation. An experimental study in rats. Haemostasis. 1976; 5: 66–73.
  13. Ehrnthaller C., Ignatius A., Gebhard F., Huber-Lang M. New insights of an old defense system: structure, function, and clinical relevance of the complement system. Mol. Med. 2011; 17: 317–329.
  14. Pöschl J.M., Leray C., Ruef P., et al. Endotoxin binding to erythrocyte membrane and erythrocyte deformability in human sepsis and in vitro. Crit. Care Med. 2003; 31: 924–928. doi: 10.1097/01.CCM.0000055366.24147.80.
  15. Lang F., Gulbins E., Lang P.A., et al. Ceramide in suicidal death of erythrocytes. Cell Physiol. Biochem. 2010; 26: 21–28. doi: 10.1159/000315102.
  16. Lang F., Qadri S.M. Mechanisms and Significance of Eryptosis, the Suicidal Death of Erythrocytes. Blood Purif. 2012; 33: 125–130. doi: 10.1159/000334163.
  17. Hod E.A., Zhang N., Sokol S.A., et al. Transfusion of red blood cells after prolonged storage produces harmful effects that are mediated by iron and inflammation. Blood. 2010; 115: 4284–4292. doi: 10.1182/blood-2009-10-245001.
  18. Dutra F.F., Bozza M.T. Heme on innate immunity and inflammation. Front. Pharmacol. 2014; 5: 115. doi: 10.3389/fphar.2014.00115.
  19. Vinchi F., Tolosano E. Therapeutic approaches to limit hemolysis-driven endothelial dysfunction: scavenging free heme to preserve vasculature homeostasis. Oxid. Med. Cell. Longev. 2013; 2013: 396527. doi: 10.1155/2013/396527.
  20. Linder M.M., Wacha H., Feldmann U., et al. The Mannheim peritonitis index. An instrument for the intraoperative prognosis of peritonitis. Chirurg. 1987; 58(2): 84–92.
  21. Singer M., Deutschman C.S., Seymour C.W., et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016; 315(8): 801–810. doi: 10.1001/jama.2016.0287.
  22. Vincent J.L., Ince C., Bakker J. Clinical review: Circulatory shock-an update: a tribute to Professor Max Harry Weil. Crit. Care. 2012; 16(6): 239. doi: 10.1186/cc11510.
  23. Савельев О.Н., Сухоруков В.П., Киселева А.В. Определение свободного гемоглобина плазмы крови гемоглобинцианидным методом. Лаб. дело. 1990; 10: 45–47. [Savelyev O.N., Sukhorukov V.P., Kiseleva A.V. Definition of free plasma hemoglobin gemoglobincianidnym method. Lab. case. 1990; 10: 45–47. (In Russ)]
  24. Мeisner M. PCT — procalcitonin. A new and innovative parameter in diagnosis of infections. Berlin: BRAHMS Diagnostica, 1996.
  25. Belcher J.D., Mahaseth H., Welch T.E., et al. Critical role of endothelial cell activation in hypoxia-induced vasoocclusion in transgenic sickle mice. American Journal of Physiology. 2005; 288(6): 2715–2725. doi: 10.1152/ajpheart.00986.2004.
  26. Belcher J.D., Mahaseth H., Welch T.E., et al. Heme oxygenase-1 is a modulator of inflammation and vaso-occlusion in transgenic sickle mice. Journal of Clinical Investigation. 2006; 116(3): 808–816. doi: 10.1172/JCI26857.
  27. Jeney V., Balla J., Yachie A., et al. Pro-oxidant and cytotoxic effects of circulating heme. Blood. 2002; 100(3): 879–887.
  28. Kumar S., Bandyopadhyay U. Free heme toxicity and its detoxification systems in human. Toxicology Letters. 2005; 157(3): 175–188. doi: 10.1016/j.toxlet.2005.03.004.
  29. Weinberg E.D. Iron and infection. Microbiol. Rev. 1978; 42(1): 45–66.
  30. Cassat J.E., Skaar E.P. Iron in Infection and Immunity. Cell. Host. Microbe. 2013; 13(5): 509–519. doi: 10.1016/j.chom.2013.04.010.
  31. Brauckmann S., Effenberger-Neidnicht K., de Groot H., et al. Lipopolysaccharide-induced hemolysis: Evidence for direct membrane interactions. Sci.Rep. 2016; 6: 35508. doi: 10.1038/srep35508.

On the diagnosis and treatment of nosocomial tracheobronchitis in intensive care medicine

A.N. Kuzovlev, A.K. Shabanov, A.V. Grechko

V.A. Negovsky research institute of general reanimatology of the Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow

For correspondence: Artem N. Kuzovlev — MD, DrMed, vice-director for science, head of the laboratory of clinical pathophysiology of critical states of the V.A. Negovsky research institute of general reanimatology Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology; Moscow; e-mail: artem_kuzovlev@mail.ru

For citation: Kuzovlev AN, Shabanov AK, Grechko AV. On the Diagnosis and Treatment of Nosocomial Tracheobronchitis in Intensive Care Medicine. Alexander Saltanov Intensive Care Herald. 2018;1:43–7.

DOI: 10.21320/1818-474X-2018-1-43-47


This review highlights the current state of the problem of nosocomial pneumonia and nosocomial tracheobronchitis. The important concept for nosocomial tracheobronchitis, the role of inhaled antibiotics in the treatment of this condition and their ability to prevent the development of nosocomial pneumonia are discussed.

Keywords: nosocomial pneumonia, nosocomial tracheobronchitis, sepsis, antibiotics, inhalation, colistin, tobramycin

Received: 04.03.2018


References

  1. Гельфанд Б.Р. Нозокомиальная пневмония у взрослых. Российские национальные рекомендации. М.: МИА, 2016. [Gelfand B.R. Nozokomialʼnaya pnevmoniya u vzroslyh. Rossijskie nacionalʼnye rekomendacii. Moscow: МIА, 2016. (In Russ)]
  2. Susan E., Coffin M.M., Klompas M., et al. Strategies to prevent ventilator‐associated pneumonia in acute care hospitals. Infection Control and Hospital Epidemiology. 2008; 29: S31–40. doi: 10.1086/591062.
  3. КузовлевА.Н., Гречко А.В. Ингаляционные антибиотики в реаниматологии: состояние, проблемы и перспективы развития. Общая реаниматология. 2017, 13(5): 69–85. [Kuzovlev A.N., Grechko A.V. Ingalyacionnye antibiotiki v reanimatologii: sostoyanie, problemy i perspektivy razvitiya. Obshchaya reanimatologiya, 2017, 13(5): 69–85. (In Russ)]. doi: dx.doi.org/10.15360/1813-9779-2017-5-69-84.
  4. Imberti R., Cusato M., Villani P., et al. Steady-state pharmacokinetics and BAL concentration of colistin in critically ill patients after IV colistin methanesulfonate administration. Chest. 2010; 138:1333–1339. doi: 10.1378/chest.10-0463.
  5. Kollef M.H., Chastre J., Clavel M., et al. A randomized trial of 7-day doripenem versus 10-day imipenem-cilastatin for ventilator- associated pneumonia. Crit. Care. 2012; 16(6): R218. doi: 10.1186/cc11862.
  6. Dulhunty J.M., Roberts J.A., Davis J.S., et al. A multicenter randomized trial of continuous versus intermittent beta-lactam infusion in severe sepsis. Am. J. Respir. Crit. Care Med. 2015; 192(11): 1298–1305. doi: 10.1164/rccm.201505–0857OC.
  7. Tamma P.D., Putcha N., Suh Y.D., et al. Does prolonged beta-lactam infusions improve clinical outcomes compared to intermittent infusions? A meta-analysis and systematic review of randomized, controlled trials. BMC Infect. Dis. 2011; 11: 181. doi: 10.1186/1471-2334-11-181.
  8. Marcus R., Paul M., Elphick H., et al. Clinical implications of beta-lactam-aminoglycoside synergism: systematic review of randomized trials. Int. J. Antimicrob. Agents. 2011; 37(6): 491–503. doi: 10.1016/j.ijantimicag.2010.11.029.
  9. Chastre J., Wolff M., Fagon J.Y., et al. Comparison of 8 vs 15 days of antibiotic therapy for ventilator-associated pneumonia in adults: a randomized trial. JAMA. 2003; 290(19): 2588–2598.
  10. Wunderink R.G. POINT: Should Inhaled Antibiotic Therapy Be Used Routinely for the Treatment of Bacterial Lower Respiratory Tract Infections in the ICU Setting? Chest. 2017; 151(4): 737–739. doi: 10.1016/j.chest.2016.11.006.
  11. Niederman M.S., Chastre J., Corkery K., et al. BAY41–6551 achieves bactericidal tracheal aspirate amikacin concentrations in mechanically ventilated patients with gram-negative pneumonia. Intensive Care Med. 2012; 38(2): 263–271. doi: 10.1007/s00134-011-2420-0.
  12. Le J., Ashley E.D., Neuhauser M.M., et al. Consensus summary of aerosolized antimicrobial agents: application of guideline criteria. Insights from the Society of Infectious Diseases Pharmacists. Pharmacotherapy 2010; 30(6): 562–584. doi: 10.1592/phco.30.6.562.
  13. Weers J. Inhaled antimicrobial therapy — barriers to effective treatment. Adv. Drug. Deliv. Rev. 2015, 85: 24–43. doi: 10.1016/j.addr.2015.04.014.
  14. Lu Q., Yang J., Liu Z., et al. Nebulized Antibiotics Study Group. Nebulized ceftazidime and amikacin in ventilator-associated pneumonia caused by Pseudomonas aeruginosa. Am. J. Respir. Crit. Care Med. 2011; 184(1): 106–115. doi: 10.1164/rccm.201011–1894OC.
  15. Ferrari F., Lu Q., Girardi C., Petitjean O., et al. Nebulized ceftazidime in experimental pneumonia caused by partially resistant Pseudomonas aeruginosa. Intensive Care Med. 2009; 35:1792–1800. doi: 10.1007/s00134-009-1605-2.
  16. Lu Q., Girardi C., Zhang M., et al. Nebulized and intravenous colistin in experimental pneumonia caused by Pseudomonas aeruginosa. Intensive Care  Med. 2010; 36: 1147–1155. doi: 10.1007/s00134-010-1879-4.
  17. Alves J., Alp E., Koulenti D., et al. Nebulization of antimicrobial agents in mechanically ventilated adults in 2017: an international cross-sectional survey. Eur. J. Clin. Microbiol. Infect. Dis. 2018; 37(4): 785–794. doi: 10.1007/s10096-017-3175-5.
  18. Rello J., Solé-Lleonart C., Rouby J.J., et al. Use of Nebulized Antimicrobials for the Treatment of Respiratory Infections in Invasively Mechanically Ventilated Adults: A Position Paper from the European Society of Clinical Microbiology and Infectious Diseases. Clin. Microbiol. Infect. 2017; 23(9): 629–639. doi: 10.1016/j.cmi.2017.04.011.
  19. Kalil A., Metersky M., Klompas M., et al. Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin. Infect. Dis. 2016; 63(5): 575–582. doi: 10.1093/cid/ciw504.
  20. А.Н.Кузовлев, А.К. Шабанов, А.М. Голубев, В.В. Мороз. Оценка эффективности ингаляционного колистина при нозокомиальной пневмонии. Общая реаниматология. 2017: 13(6): 60–74. [A.N. Kuzovlev, A.K. Shabanov, A.M. Golubev, V.V. Moroz. Ocenka ehffektivnosti ingalyacionnogo kolistina pri nozokomialʼnoj pnevmonii. Obshchaya reanimatologiya. 2017; 13(6): 60–74. (In Russ)] doi: dx.doi.org/10.15360/1813-9779-2017-6-60-73.
  21. КузовлевА.Н., Мороз В.В., Голубев А.М. Ингаляционные антибиотики в лечении нозокомиальной пневмонии. Анестезиология и реаниматология. 2015; 4: 68–74.
  22. Karvouniaris M., Makris D., Manoulakas E., et al. Ventilator-associated tracheobronchitis increases the length of intensive care unit stay. Infect. Control. Hosp. Epidemiol. 2013; 34(8): 800–808. doi: 10.1086/671274.
  23. Martin-Loeches I., Povoa P., Rodríguez A., et al. TAVeM study. Incidence and prognosis of ventilator-associated tracheobronchitis (TAVeM): a multicentre, prospective, observational study. Lancet Respir. Med. 2015; 3(11): 859–868. doi: 10.1016/S2213–2600(15)00326–4.
  24. Craven D.E., Lei Y., Ruthazer R., et al. Incidence and outcomes of ventilator-associated tracheobronchitis and pneumonia. Am. J. Med. 2013; 126: 542–549. doi: 10.1016/j.amjmed.2012.12.012.
  25. Nseir S., Deplanque X., Di Pompeo C., et al. A Risk factors for relapse of ventilator-associated pneumonia related to nonfermenting Gram negative bacilli: a case–control study. J. Infect. 2008; 56: 319–325. doi: 10.1016/j.jinf.2008.02.012.
  26. Luna C.M., Aruj P., Niederman M.S., et al. Appropriateness and delay to initiate therapy in ventilator-associated pneumonia. Eur. Respir. J. 2006, 27: 158–164.
  27. Palmer L.B., Smaldone G.C., Chen J.J., et al. Aerosolized antibiotics and ventilator-associated tracheobronchitis in the intensive care unit. Crit. Care Med. 2008, 36(7): 2008–2013. doi: 10.1097/CCM.0b013e31817c0f9e.
  28. Nseir S., Favory R., Jozefowicz E., et al. Antimicrobial treatment for ventilator-associated tracheobronchitis: a randomized, controlled, multicenter study. Crit. Care. 2008, 12(3): R62. doi: 10.1186/cc13940.
  29. Claridge J.A., Edwards N.M., Swanson J., et al. Aerosolized ceftazidime prophylaxis against ventilator-associated pneumonia in high-risk trauma patients: results of a double-blind randomized study. Surg. Infect. (Larchmt). 2007; 8(1): 83–90. doi: 10.1089/sur.2006.042.
  30. Karvouniaris M., Makris D., Zygoulis P., et al. Nebulized colistin for ventilator-associated pneumonia prevention. Eur. Respir. J. 2015; 46(6): 1732–1739. doi: 10.1183/13993003.02235–2014.
  31. Russell C.J., Shiroishi M.S., Siantz E., et al. The use of inhaled antibiotic therapy in the treatment of ventilator-associated pneumonia and tracheobronchitis: a systematic review. BMC Pulm. Med. 2016; 16: 40. doi: 10.1186/s12890-016-0202-8.
  32. Póvoa F.C.C., Cardinal-Fernandez P., Maia I.S., et al. Effect of antibiotics administered via the respiratory tract in the prevention of ventilator-associated pneumonia: A systematic review and meta-analysis. J.Crit. Care. 2018; 43: 240–245. doi: 10.1016/j.jcrc.2017.09.019.