Changes in the pituitary-adrenal system for extracorporal membrane oxygenation: prospective study
ISSN (print) 1726-9806     ISSN (online) 1818-474X
#3 2022
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Keywords

critical illness
hydrocortisone
cortisol
extracorporeal membrane oxygenation
adrenal glands
adrenocorticotropic hormone

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1.
Altshuler N.E., Kutcyi M.B., Kruglyakov N.M., Gubarev K.K., Bagzhanov G.I., Popugaev K.A. Changes in the pituitary-adrenal system for extracorporal membrane oxygenation: prospective study. Annals of Critical Care. 2022;(3):69-81. doi:10.21320/1818-474X-2022-3-69-81

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Abstract

INTRODUCTION. At the moment, assessing adrenal dysfunction in critical patients and ways to correct this function with hormone replacement therapy are extremely difficult. OBJECTIVES. Analysis of changes in the dynamics of ACTH and cortisol levels in blood plasma during ECMO. MATERIALS AND METHODS. The prospective study was performed in intensive care unit (47 patients on ECMO). After connecting ECMO (D0), (D1–D3–D5–D7–D9), and until the completion of ECMO, assessment of cortisol and ACTH levels was carried out. RESULTS. The median level of cortisol in blood plasma was higher in the non-survivors patients on the third day (D3) (p = 0.05), D7 (p = 0.03); D13 (p = 0.05) and the last day of observation (p = 0.001), respectively. The level of ACTH in the blood of non-survivors patients was higher immediately on the day of ECMO initiation (D0) and on day 3 (D3) of observation: D0 (p = 0.018); D3 (p = 0.04), respectively. Analysis of the ROC curve showed that cortisol levels show a sensitivity of 71 % and a specificity of 89 % to an adverse outcome during ECMO. DISCUSSION. The life-saving ECMO technique, in critical conditions, is associated with a high risk of increasing of complications, including potentially lethal ones. Critical illness-related corticosteroid insufficiency (CIRCI) clinically manifests itself as inadequate adrenal activity, taking into account the augmentation of the disease severity. This activity is expressed in the form of a decrease in production and/or resistance to endogenous cortisol, as confirmed by the study. Consideration of CIRCI during the usage of ECMO reflects more objectively the violation of the pituitary-adrenal system. CONCLUSIONS. 1. CIRCI is detected in patients during ECMO. 2. High plasma cortisol levels are the predictor of an adverse outcome. 3. The level of ACTH in blood plasma is higher in patients with adverse outcomes. 4. High levels of cortisol in plasma are not a criterion for making the decision to initiate hydrocortisone therapy.

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References

  1. Шанин В.Ю. Патофизиология критических состояний. СПб.: Элби-СПб, 2003. [Shanin V.U. Pathophysiology of critical conditions. SPb.: Elbi-SPb, 2003. (In Russ)]
  2. Рябов Г.А. Гипоксия критических состояний. М.: Медицина, 1988. [Ryabov G.A. Hypoxia of critical conditions. M.: Medicine, 1988. (In Russ)]
  3. Boonen E., Van den Berghe G.V. Endocrine responses to critical illness: novel insights and therapeutic implications. J Clin Endocrinol Metab. 2014; 99(5): 1569–82. DOI: 10.1210/jc.2013-4115
  4. Молотков О.В., Ефременков С.В., Решедько В.В. Патофизиология в вопросах и ответах: учебное пособие. Смоленск: САУ, 1999. [Molotkov O.V., Efremenko S.V., Reshedko V.V. Pathophysiology in questions and answers: study guide. Smolensk: SAU, 1999. (In Russ)]
  5. Akrout N., Sharshar T., Annane D. Mechanisms of brain signaling during sepsis. Curr Neuropharmacol. 2009; 7(4): 296–301. DOI: 10.2174/157015909790031175
  6. Téblick A., Peeters B., Langouche L., et al. Adrenal function and dysfunction in critically ill patients. Nat Rev Endocrinol. 2019; 15(7): 417–27. DOI: 10.1038/s41574-019-0185-7
  7. Van den Berghe G., de Zegher F., Veldhuis J.D., et al. Thyrotrophin and prolactin release in prolonged critical illness: dynamics of spontaneous secretion and effects of growth hormone secretagogues. Clin Endocrinol (Oxf). 1997; 47: 599–612. DOI: 10.1046/j.1365-2265.1997.3371118.x
  8. Marik P.E., Pastores S.M., Annane D., et al. Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients: consensus statements from an international task force by the American College of Critical Care Medicine. Crit Care Med. 2008; 36(6): 1937–49. DOI: 10.1097/ccm.0b013e31817603ba
  9. Евдокимова Е.А., Власенко А.В., Авдеева С.Н. Респираторная поддержка пациентов в критическом состоянии. М.: ГЭОТАР-Медиа, 2021. [Evdokimova E.A., Vlasenko A.V., Avdeeva S.N. Respiratory support for patients in critical condition. M.: GEOTAR-Media, 2021. (In Russ)]
  10. Millar J.E., Fanning J.P., McDonald C.I., et al. The inflammatory response to extracorporeal membrane oxygenation (ECMO): a review of the pathophysiology. Crit Care. 2016; 20: 387. DOI: 10.1186/s13054-016-1570-4
  11. Bonnemain J., Rusca M., Ltaief Z., et al. Hyperoxia during extracorporeal cardiopulmonary resuscitation for refractory cardiac arrest is associated with severe circulatory failure and increased mortality. BMC Cardiovasc Disord. 2021; 21: 542. DOI: 10.1186/s12872-021-02361-3
  12. Appelt H., Philipp A., Mueller T., et al. Factors associated with hemolysis during extracorporeal membrane oxygenation (ECMO)—Comparison of VA-versus VV ECMO. PLoS ONE. 2020; 15(1): e0227793. DOI: 10.1371/journal.pone.0227793
  13. Sauneuf B., Chudeau N., Champigneulle B., et al. Pheochromocytoma crisis in the ICU: a french multicenter cohort study with emphasis on rescue extracorporeal membrane oxygenation. Crit Care Med. 2017; 45(7): e657–e665. DOI: 10.1097/CCM.0000000000002333
  14. Chao A., Wang C.H., You H.C., et al. Highlighting indication of extracorporeal membrane oxygenation in endocrine emergencies. Sci Rep. 2015; 5: 13361. DOI: 10.1038/srep13361
  15. Combes A., Hajage D., Capellier G. Extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. N Engl J Med. 2018; 378(21): 1965–75. DOI: 10.1056/NEJMoa1800385
  16. Ferguson N.D., Fan E., Camporota L., et al. The Berlin definition of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med. 2012; 38(10): 1573–82. DOI: 10.1007/s00134-012-2682-1
  17. Braune S., Sieweke A., Brettner F., et al. The feasibility and safety of extracorporeal carbon dioxide removal to avoid intubation in patients with COPD unresponsive to noninvasive ventilation for acute hypercapnic respiratory failure (ECLAIR study): multicentre case-control study. Intensive Care Med. 2016; 42: 1437–44. DOI: 10.1007/s00134-016-4452-y
  18. Ouweneel D.M., Schotborgh J.V., Limpens J., et al. Extracorporeal life support during cardiac arrest and cardiogenic shock: a systematic review and meta-analysis. Intensive Care Med. 2016; 42: 1922–34. DOI: 10.1007/s00134-016-4536-8
  19. Debaty G., Babaz V., Durand M., et al. Prognostic factors for extracorporeal cardiopulmonary resuscitation recipients following out-of-hospital refractory cardiac arrest. A systematic review and meta-analysis. Resuscitation. 2017; 112: 1–10. DOI: 10.1016/j.resuscitation.2016.12.011
  20. Broman L.M., Malfertheiner M.V., Montisci A., et al. Weaning from veno-venous extracorporeal membrane oxygenation: how I do it. J Thorac Dis. 2018; 10(5): S692–S697. DOI: 10.21037/jtd.2017.09.95
  21. Vasques F., Romitti F., Gattinoni L., et al. How I wean patients from veno-venous extra-corporeal membrane oxygenation. Crit Care. 2019; 23(1): 316. DOI: 10.1186/s13054-019-2592-5
  22. Fried J.A., Masoumi A., Takeda K., et al. How I approach weaning from venoarterial ECMO. Crit Care. 2020; 24(1): 307. DOI: 10.1186/s13054-020-03010-5
  23. Annane D., Bellissant E., Bollaert P.E., et al. Corticosteroids for treating sepsis. Cochrane Database Syst Rev. 2015; 12: CD002243. DOI: 10.1002/14651858.CD002243.pub3
  24. Rubartelli A., Lotze M.T. Inside, outside, upside down: damage-associated molecular-pattern molecules (DAMPs) and redox. Trends Immunol. 2007; 28(10): 429–36. DOI: 10.1016/j.it.2007.08.004
  25. Zindel J, Kubes P. DAMPs, PAMPs, and LAMPs in immunity and sterile inflammation. Annu Rev Pathol. 2020; 15:493-18. DOI: 10.1146/annurev-pathmechdis-012419-032847.
  26. Шмидт Р.В., Ланг Ф., Хекманн М. Физиология человека с основами патофизиологии. М.: Лаборатория знаний, 2011. [Schmidt R.V., Lang F., Heckmann M. Human physiology with the basics of pathophysiology. M.: Laboratory of Knowledge, 2011. (In Russ)]
  27. Топический диагноз вневрологии по Петеру Дуусу. Анатомия. Физиология. Клиника. Под ред. М. Бера, М. Фротшера; пер. с англ. под ред. О.С. Левина. М.: Практическая медицина, 2018. [Duus’ Topical Diagnosis in Neurology. Anatomy. Physiology. Clinic. Ed. by M. Ber, M. Froshter; Transl. from Engl. Ed. by OS. Levin. M.: Practical Medicine, 2018. (In Russ)]
  28. Кирячков Ю.Ю., Босенко С.А., Муслимов Б.Г. идр. Дисфункция автономной нервной системы в патогенезе септических критических состояний (обзор). Современные технологии медицины. 2020; 4: 106–18. DOI: 17691/stm2020.12.4.12 [Kiryachkov Yu.Yu., Bosenko S.A., Muslimov B.G., et al. Dysfunction of the autonomic nervous system in the pathogenesis of septic critical conditions (review). Sovremennye tekhnologii mediciny. 2020; 4: 106–18. DOI: 10.17691/stm2020.12.4.12 (In Russ)]
  29. Мелмед Ш., Полонски К.С., Ларсен П.Р. идр. Эндокринология по Вильямсу. Нейроэндокринология. Под ред. И.И. Дедова, Г.А. Мельниченко. М.: ГЭОТАР-Медиа, 2019. [Melmed S., Polonsky K.S., Larsen P.R., et al. Endocrinology according to Williams. Neuroendocrinology. Ed. by I.I. Dedov, G.A. Melnichenko. M.: GEOTAR-Media, 2019. (In Russ)]
  30. Qian Y.S., Zhao Q.Y., Zhang S.J., et al. Effect of α7nAChR mediated cholinergic anti-inflammatory pathway on inhibition of atrial fibrillation by low-level vagus nerve stimulation. Zhonghua Yi Xue Za Zhi. 2018; 98(11): 855–9. DOI: 10.3760/cma.j.issn.0376-2491.2018.11.013
  31. Deussing J., Chen А. The corticotropin-releasing factor family: physiology of the stress response. Physiological Reviews. 2018; 98: 2225–86. DOI: 10.1152/physrev.00042.2017
  32. Тучина О.П. Нейро-иммунные взаимодействия в холинергическом противовоспалительном пути. Гены и клетки. 2020; 15(1): 23–8. DOI: 10.23868/202003003 [Tuchina O.P. Neuro-immune interactions in the cholinergic anti-inflammatory pathway. Geny i kletki. 2020; 15(1): 23–8. DOI: 10.23868/202003003 (In Russ)]
  33. Горбачев В.И., Брагина Н.В. Гематоэнцефалический барьер с позиции анестезиолога- реаниматолога: Обзор литературы. Ч. 2. Вестник интенсивной терапии им. А.И. Салтанова. 2020; 3: 46–55. DOI: 10.21320/1818-474X-2020-3-46-55 [Gorbachev V.I., Bragina N.V. The blood-brain barrier from the position of an anesthesiologist- resuscitator. Literature review. Part 2. Bulletin of Intensive Care named after A.I. Saltanov. 2020; 3: 46–55. DOI: 10.21320/1818-474X-2020-3-46-55 (In Russ)]
  34. Galiano M., Liu Z.Q., Kalla R., et al. Interleukin-6 (IL6) and cellular response to facial nerve injury: effects on lymphocyte recruitment, early microglial activation and axonal outgrowth in IL6-deficient mice. Eur J Neurosci. 2001; 14: 327–41. DOI: 10.1046/j.0953-816x.2001.01647.x
  35. Peeters B., Langouche L., Van den Berghe G. Adrenocortical Stress Response during the Course of Critical Illness. Compr Physiol. 2017; 8(1): 283–98. DOI: 10.1002/cphy.c170022
  36. Tominaga T., Fukata J., Naito Y., et al. Prostaglandin-dependent in vitro stimulation of adrenocortical steroidogenesis by interleukins. Endocrinology. 1991; 128(1): 526–31. DOI: 10.1210/endo-128-1-526
  37. Меркулов В.М., Меркулова Т.И. Изоформы рецептора глюкокортикоидов, образующиеся в результате альтернативного сплайсинга и использования альтернативных стартов трансляции МРНК. Вавиловский журнал генетики и селекции. 2011; 15(4): 631–2. [Merkulov V.M., Merkulova T.I. Isoforms of the glucocorticoid receptor formed as a result of alternative splicing and the use of alternative MRNA translation starts. Vavilovskij zhurnal genetiki i selekcii. 2011; 15(4): 631–2. (In Russ)]
  38. Arlt W., Allolio B. Adrenal insufficiency. Lancet. 2003; 361(9372): 1881–93. DOI: 10.1016/S0140-6736(03)13492-7
  39. Annane D., Pastores S.M., Rochwerg B., et al. Guidelines for the diagnosis and management of critical illness-related corticosteroid insufficiency (CIRCI) in Critically Ill Patients (Part I): society of Critical Care Medicine (SCCM) and European Society of Intensive Care Medicine (ESICM). Crit Care Med. 2017; 45(12): 2078–88. DOI: 10.1097/CCM.0000000000002737
  40. Фадеев В.В., Мельниченко Г.А. Надпочечниковая недостаточность (клиника, диагностика, лечение): методические рекомендации для врачей. М.: Медпрактика-М, 2003. [Fadeev V.V., Melnichenko G.A. Adrenal insufficiency (clinic, diagnosis, treatment): methodical recommendations for doctors. M.: Medpraktika-M, 2003. (In Russ)]
  41. Nickler M., Ottiger M., Steuer C., et al. Time-dependent association of glucocorticoids with adverse outcome in community-acquired pneumonia: a 6-year prospective cohort study. Critical Care. 2017; 21: 72. DOI: 10.1186/s13054-017-1656-7
  42. Annane D., Sebille V., Troche G., et al. A 3-level prognostic classification in septic shock based on cortisol levels and cortisol response to corticotropin. JAMA. 2000; 283(8): 1038–45. DOI: 10.1001/jama.283.8.1038
  43. Sam S., Corbridge T.C., Mokhlesi B., et al. Cortisol levels and mortality in severe sepsis. Clin Endocrinol (Oxf). 2004; 60(1): 29–35. DOI: 10.1111/j.1365-2265.2004.01923.x
  44. Schein R.M., Sprung C.L., Marcial E., et al. Plasma cortisol levels in patients with septic shock. Crit Care Med. 1990; 18(3): 259–63. DOI: 10.1097/00003246-199003000-00002
  45. Cohen J., Pretorius C.J., Ungerer J.P., et al. Glucocorticoid sensitivity is highly variable in critically ill patients with septic shock and is associated with disease severity. Crit. Care Med. 2016; 44: 1034–41. DOI: 10.1097/CCM.0000000000001633
  46. Alder M.N., Opoka A.M., Wong H.R. The glucocorticoid receptor and cortisol levels in pediatric septic shock. Crit. Care. 2018; 22: 244. DOI: 10.1186/s13054-018-2177-8
  47. Jenniskens M., Weckx R., Dufour T., et al. The hepatic glucocorticoid receptor is crucial for cortisol homeostasis and sepsis survival in humans and Male mice. Endocrinology. 2018; 159: 2790–802. DOI: 10.1210/en.2018-00344
  48. Abraham M.N., Jimenez D.M., Fernandes T.D., et al. Cecal ligation and puncture alters glucocorticoid receptor expression. Crit Care Med. 2018; 46: 797–804. DOI: 10.1097/CCM.0000000000003201
  49. Dendoncker K., Libert C. Glucocorticoid resistance as a major drive in sepsis pathology. Cytokine Growth Factor Rev. 2017; 35: 85–96. DOI: 10.1016/j.cytogfr.2017.04.002
  50. Wasyluk W., Wasyluk M., Zwolak A. Sepsis as a pan-endocrine illness-endocrine disorders in septic patients. J Clin Med. 2021; 10(10): 2075. DOI: 10.3390/jcm10102075
  51. Lewis-Tuffin L.J., Cidlowski J.A. The physiology of human glucocorticoid receptor beta (hGRbeta) and glucocorticoid resistance. Ann N Y Acad Sci. 2006; 1069: 1–9. DOI: 10.1196/annals.1351.001
  52. Schaaf M.J., Cidlowski J.A. Molecular mechanisms of glucocorticoid action and resistance. J Steroid Biochem Mol Biol. 2002; 83: 37–4. DOI: 10.1016/s0960-0760(02)00263-7
  53. Ярошецкий А.И., Грицан А.И., Авдеев С.Н. и др. Диагностика и интенсивная терапия острого респираторного дистресс-синдрома. Анестезиология и реаниматология. 2020; 2: 5–39. DOI: 17116/anaesthesiology20200215 [Yaroshetsky A.I., Gritsan A.I., Avdeev S.N., et al. Diagnostics and intensive therapy of Acute Respiratory Distress Syndrome (Clinical guidelines of the Federation of Anesthesiologists and Reanimatologists of Russia). Russian Journal of Anaesthesiology and Reanimatology. 2020; 2: 5–39. DOI: 10.17116/anaesthesiology20200215 (In Russ)]
  54. Vincent J.L., Quintairos E., Silva A., et al. The value of blood lactate kinetics in critically ill patients: a systematic review. Crit Care. 2016; 20(1): 257. DOI: 10.1186/s13054-016-1403-5
  55. Levy-Shraga Y., Pinhas-Hamiel O., Molina-Hazan V., et al. Elevated baseline cortisol levels are predictive of bad outcomes in critically ill children. Pediatric Emergency Care. 2018; 34(9): 613–7. DOI: 10.1097/PEC.0000000000000784
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