Hubungan Kadar Serum Kortisol Awal dengan Kejadian Infeksi pada Stroke Akut di RSUD Dr. Soetomo Surabaya

Indah Ari Handaayani*, J. Ekowahono**
* Peserta PPDS-1 Neurologi FK Unair/RSUD Dr.Soetomo Surabaya
** Staf Pengajar Departemen/SMF Neurologi FK Unair/RSUD Dr.Soetomo Surabaya

Abstract

         Latar Belakang dan Tujuan. Komplikasi infeksi pada stroke merupakan masalah utama dalam perawatan penderita stroke karena menentukan prognosis. Perubahan endokrin berupa kortisol adalah salah satu perubahan yang dapat diukur sebagai respon terhadap stress pada stroke akut. Pada fase akut kortisol bersifat sebagai pro inflamasi, tetapi pada kadar semakin tinggi kortisol menyebabkan terjadinya penurunan sistem imun sehingga penderita rentan mengalami infeksi. Tujuan penelitian ini adalah untuk mengetahui hubungan antara kadar serum kortisol awal dengan kejadian infeksi pada penderita stroke akut. Metode. Studi kohort prospektif dilakukan pada 32 penderita stroke akut yang datang di ruang Seruni, Seruni A, dan Seruni B RSUD Dr. Soetomo Surabaya dan memenuhi kriteria inklusi-eksklusi selama periode Desember 2015- Februari 2016. Sebanyak 2 cc darah vena dalam 48 jam sejak awitan stroke, diperiksa kadar kortisol serum pada pukul 06.00-08.00. Selama 7 hari perawatan di rumah sakit, penderita diobservasi dan diamati tanda-tanda infeksi, baik secara klinis maupun dengan pemeriksaan penunjang sesuai dengan definisi operasional. Hasil. Pada kelompok dengan infeksi didapatkan 8 orang (50%) dengan kadar kortisol tinggi (p=0,015; RR 15,000; IK 95% 1,583–143,171); 6 orang (50%) dengan penggunaan kateter urine (p=0,049; RR 6,667; IK 95% 1,067–30,085); dan 6 orang (54,5%) menggunakan NGT (p=0,035; RR 7,200; IK 95% 1,311 – 39,557). Pada analisa multivariate didapatkan Odds Ratio (OR) 15,468 berdasarkan kadar kortisol tinggi dan OR 7,469 berdasarkan pemakaian NGT. Kesimpulan. Kadar kortisol tinggi dan pemakaian NGT berpengaruh terhadap kejadian infeksi pada stroke akut dengan kekuatan hubungan terbesar adalah kadar kortisol dengan nilai OR=15,468.

Kata kunci : stroke akut, kadar kortisol, kejadian infeksi

Daftar Pustaka

  1. Kesehatan D and RI KK. Riset Kesehatan Dasar. Jakarta: Badan Penelitian dan Pengembangan Kesehatan Departemen Kesehatan Republik Indonesia. 2013.
  2. Yudiarto F, Machfoed M, Darwin A, Ong A and Karyana M. Indonesia Stroke Registry (S12. 003). Neurology. 2014; 82: S12. 003-S12. .
  3. Elenkov IJ, Wilder RL, Chrousos GP and Vizi ES. The sympathetic nerve—an integrative interface between two supersystems: the brain and the immune system. Pharmacological reviews. 2000; 52: 595-638.
  4. Chamorro Á, Urra X and Planas AM. Infection after acute ischemic stroke a manifestation of brain-induced immunodepression. Stroke. 2007; 38: 1097-103.
  5. McEwen BS. Physiology and neurobiology of stress and adaptation: central role of the brain. Physiological reviews. 2007; 87: 873-904.
  6. Smith SM and Vale WW. The role of the hypothalamic-pituitary-adrenal axis in neuroendocrine responses to stress. Dialogues in clinical neuroscience. 2006; 8: 383.
  7. Whyte DG and Johnson AK. Lesions of the anteroventral third ventricle region exaggerate neuroendocrine and thermogenic but not behavioral responses to a novel environment. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2007; 292: R137-R42.
  8. Dirnagl U, Klehmet J, Braun JS, et al. Stroke-induced immunodepression experimental evidence and clinical relevance. Stroke. 2007; 38: 770-3.
  9. Olsson T, Marklund N, Gustafson Y and Näsman B. Abnormalities at different levels of the hypothalamic-pituitary-adrenocortical axis early after stroke. Stroke. 1992; 23: 1573-6.
  10. Fassbender K, Schmidt R, Mössner R, Daffertshofer M and Hennerici M. Pattern of activation of the hypothalamic-pituitary-adrenal axis in acute stroke. Relation to acute confusional state, extent of brain damage, and clinical outcome. Stroke. 1994; 25: 1105-8.
  11. Cranston CC. A Review of the Effects of Prolonged Exposure to Cortisol on the Regulation of the HPA Axis: Implications for the Development and Maintenance of Posttraumatic Stress Disorder. The New School Psychology Bulletin. 2014; 11: 1-13.
  12. Bishop M, Fody EP and Schoeff LE. Clinical chemistry–principles, procedures, correlation. Quality assurance. 2005; 3: 4.
  13. Fiorentino L, Saxbe D, Alessi CA, Woods DL and Martin JL. Diurnal cortisol and functional outcomes in post-acute rehabilitation patients. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences. 2012: glr230.
  14. Barugh AJ, Gray P, Shenkin SD, MacLullich AMJ and Mead GE. Cortisol levels and the severity and outcomes of acute stroke: a systematic review. Journal of neurology. 2014; 261: 533-45.
  15. N Hadlow SC, R Wardrop, D Henley. Variation of Serum Cortisol with Age and Gender. 2011.
  16. Slowik A, Turaj W, Pankiewicz J, Dziedzic T, Szermer P and Szczudlik A. Hypercortisolemia in acute stroke is related to the inflammatory response. Journal of the neurological sciences. 2002; 196: 27-32.
  17. Urra X, Cervera Á, Obach V, Climent N, Planas AM and Chamorro Á. Monocytes are major players in the prognosis and risk of infection after acute stroke. Stroke. 2009; 40: 1262-8.
  18. Wilckens T and De Rijk R. Glucocorticoids and immune function: unknown dimensions and new frontiers. Immunology today. 1997; 18: 418-24.
  19. Kumar S, Selim MH and Caplan LR. Medical complications after stroke. The Lancet Neurology. 2010; 9: 105-18.
  20. Vermeij FH, Scholte op Reimer W, De Man P, et al. Stroke-associated infection is an independent risk factor for poor outcome after acute ischemic stroke: data from the Netherlands Stroke Survey. Cerebrovascular Diseases. 2009; 27: 465-71.
  21. Aslanyan S, Weir C, Diener HC, Kaste M and Lees KR. Pneumonia and urinary tract infection after acute ischaemic stroke: a tertiary analysis of the GAIN International trial. European Journal of Neurology. 2004; 11: 49-53.
  22. Emsley HC and Hopkins SJ. Acute ischaemic stroke and infection: recent and emerging concepts. The Lancet Neurology. 2008; 7: 341-53.
  23. Hadlow N CS, Wardrop R, and Henley D. Variation of Serum Cortisol with Age and Gender. Western Diagnostic Pathology. 2011.
  24. Bouma EM, Riese H, Ormel J, Verhulst FC and Oldehinkel AJ. Adolescents’ cortisol responses to awakening and social stress; effects of gender, menstrual phase and oral contraceptives. The TRAILS study. Psychoneuroendocrinology. 2009; 34: 884-93.
  25. Christensen H. Acute stroke–a dynamic process. Dan Med Bull. 2007; 54: 210-25.
  26. Marklund N, Peltonen M, Nilsson T and Olsson T. Low and high circulating cortisol levels predict mortality and cognitive dysfunction early after stroke. Journal of internal medicine. 2004; 256: 15-21.
  27. Chiodini I, Adda G, Scillitani A, et al. Cortisol secretion in patients with type 2 diabetes relationship with chronic complications. Diabetes Care. 2007; 30: 83-8.
  28. Hammer F and Stewart PM. Cortisol metabolism in hypertension. Best Practice & Research Clinical Endocrinology & Metabolism. 2006; 20: 337-53.
  29. Warren JW. Catheter-associated urinary tract infections. International journal of antimicrobial agents. 2001; 17: 299-303.
  30. Dziewas R, Ritter M, Schilling M, et al. Pneumonia in acute stroke patients fed by nasogastric tube. Journal of Neurology, Neurosurgery & Psychiatry. 2004; 75: 852-6.
  31. Prass K, Meisel C, Höflich C, et al. Stroke-induced immunodeficiency promotes spontaneous bacterial infections and is mediated by sympathetic activation reversal by poststroke T helper cell type 1–like immunostimulation. The Journal of experimental medicine. 2003; 198: 725-36.
  32. Vogelgesang A, Grunwald U, Langner S, et al. Analysis of lymphocyte subsets in patients with stroke and their influence on infection after stroke. Stroke. 2008; 39: 237-41.
  33. Choi J, Fauce SR and Effros RB. Reduced telomerase activity in human T lymphocytes exposed to cortisol. Brain, behavior, and immunity. 2008; 22: 600-5.
  34. Mavoungou E, Bouyou‐Akotet M and Kremsner P. Effects of prolactin and cortisol on natural killer (NK) cell surface expression and function of human natural cytotoxicity receptors (NKp46, NKp44 and NKp30). Clinical & Experimental Immunology. 2005; 139: 287-96.
  35. Dimopoulou I, Kouyialis AT, Orfanos S, et al. Endocrine alterations in critically III patients with stroke during the early recovery period. Neurocritical care. 2005; 3: 224-9.
  36. Sundbøll J, Horváth-Puhó E, Schmidt M, et al. Preadmission Use of Glucocorticoids and 30-Day Mortality After Stroke. Stroke. 2016; 47: 829-35.
  37. Chamorro A, Horcajada J, Obach V, et al. The early systemic prophylaxis of infection after stroke study a randomized clinical trial. Stroke. 2005; 36: 1495-500.