YANIK TÜRÜNE GÖRE ASPARTAT TRANSAMİNAZ, ALANİN TRANSAMİNAZ VE KREATİNİN FOSFOKİNAZ DÜZEYLERİ VE TEDAVİ SÜRECİNDEKİ SEYRİ
Abstract
Giriş: Yanık cilt hasarı dışında pek çok organı etkileyebilen, kompleks mediatör sistemlerinin aktive olması ile patofizyolojik değişikliklere neden olan bir durumdur. Çalışmada yanık yoğun bakımında takip edilen hastalarda yanık türüne göre aspartat aminotransferaz, alanin aminotransferaz ve kreatinin fosfokinaz enzim düzeylerinin seyri ve doku hasarının düzeyini belirlemek amaçlanmıştır.
Yöntemler: XXXXXX XXXXX XXXX Yanık Merkezi Yanık Yoğun Bakımında XXXX XXXXX XXXXX tarihleri arasında yanık sonrası 24 saat içinde yoğun bakıma yatışı yapılan 18 yaş üzeri hastaların yaş ve cinsiyet gibi demografik verilerine ek olarak yanık tipleri kayıt edildi. Kronik hastalık öyküsü, mükerrer yatışı bulunan ve hospitalizasyon süresi 5 günün altında olan hastalar kapsam dışı tutuldu. Hastaların yatışlarının bir, üç ve beşinci gününde aspartat aminotransferaz, alanin aminotransferaz ve kreatinin fosfokinaz düzeyleri değerlendirildi.
Bulgular: Çalışma kapsamına alınan 132 hastanın 95’i (%71.9) erkek cinsiyette olup, ortanca yaş 35 (18-92) yıl olarak saptandı. Yanık tipine göre; elektrik akımına maruziyet ile yanık 20, alev yanığı 38, haşlanma yanığı 43, temas yanığı 12, kimyasal yanık 4, alev+inhalasyon yanığı 14 olarak saptandı. Yalnızca elektrik akımı yanıkları ve alev-inhalasyon yanık hastalarında yatış anında ve takipte aspartat aminotransferaz, alanin aminotransferaz ve kreatinin fosfokinaz düzeyleri yüksekti (p<0,05).
Sonuç: Bu çalışmada elektrik yanıklarında en yüksek doku hasarı gözlenmiş olup, alev inhalasyon tipi yanıklarda ise karaciğer ve iskelet kası hipoksisine bağlı aspartat aminotransferaz, alanin aminotransferaz ve kreatinin fosfokinaz düzeylerinin arttığı söylenebilir. Her yanık türünün kendine özgü hasarı, takibi ve tedavisi vardır. Bu çalışma ile yanık tipine göre doku hasarı değerlendirilerek yanık türüne göre takip ve uygulanacak tedavilere katkı sağlayacağına inanıyoruz.
References
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ASPARTATE TRANSAMINASE, ALANINE TRANSAMINASE AND CREATININE PHOSPHOKINASE LEVELS ACCORDING TO BURN TYPE AND COURSE OF TREATMENT
Abstract
Introduction: Burn is a condition that can affect many organs other than skin damage and causes pathophysiological changes with the activation of complex mediator systems. This study aimed to determine the course of aspartate aminotransferase, alanine aminotransferase, and creatinine phosphokinase enzyme levels and the level of tissue damage according to burn type in patients followed up in the burn intensive care unit.
Methods: In addition to demographic data such as age and gender, burn types of patients over 18 years of age who were admitted to the intensive care unit within 24 hours after burns in the Burn Intensive Care Unit of XXXXXX XXXXX XXXX Burn Centre between XXXX XXXXX XXXXX dates were recorded. Patients with a history of chronic disease, repeated hospitalizations, and a hospitalization period of fewer than 5 days were excluded from the study. Aspartate aminotransferase, alanine aminotransferase, and creatinine phosphokinase levels were evaluated on hospitalization's first, third, and fifth days.
Results: Of the 132 patients included in the study, 95 (71.9%) were male and the median age was 35 (18-92) years. According to burn type; electric current burn 20, flame burns 38, scald burn 43, contact burn 12, chemical burn 4, and flame+inhalation burn 14. Aspartate aminotransferase, alanine aminotransferase, and creatinine phosphokinase levels were elevated only in patients with electric current burns and flame-inhalation burns during hospitalization and follow-up (p<0.05).
Conclusion: In this study, the highest tissue damage was observed in electrical burns, and in flame inhalation type burns, aspartate aminotransferase, alanine aminotransferase, and creatinine phosphokinase levels increased due to the liver and skeletal muscle hypoxia. Each burn type has its damage, follow-up, and treatment. We believe that this study will contribute to the follow-up and treatments to be applied according to burn type by evaluating tissue damage according to burn type.
Keywords
Aspartate aminotransferase Alanine aminotransferase Creatinine phosphokinase Tissue damage Burn
References
- 1. Masood RA, Wain ZN, Tariq R, et al. Burn Cases, Their Management and Complications: A Review. Int Curr Pharm J. 2016;5:103-5.
- 2. Göksel Ş, Şehirli AÖ, Şatıroğlu H, et al. Melatonin improves oxidative organ damage in a rat model of thermal injury. Burns. 2002;28:419-25.
- 3. Lalonde C, Knox J, Youn YK, et al. Relationship between hepatic blood flow and tissue lipid peroxidation in the early postburn period. Crit Care Med. 1992;20:789-96.
- 4. Mandell SP, Gibran NS. Early enteral nutrition for burn injury. Adv Wound Care. 2014;3:64-70.
- 5. Brusselaers N, Monstrey S, Vogelaers D et al. Severe burn injury in Europe: A systematic review of the incidence, etiology, morbidity, and mortality. Crit Care. 2010;14:188.
- 6. Erkuran MK, Ceylan A, Düzenli E, Büyükcam F. Şanlıurfa Eğitim ve Araştırma Hastanesi’nde Yatırılarak İzlenmiş Olan Yanık Vakaları. Abant Med J. 2013;2:123-9.
- 7.Papini, R. Management of burn injuries of various depths. British Med J. 2004;329:158-60.
- 8. Demling R, Desanti L. Burns: Resustation phase. In: Hall JB, Schmidt GA, Wood L, editors. Principles of critical care. USA; MG. Hill; 2005. P. 1457-65.
- 9.Youn YK, Suh GJ, Jung SE, et al. Recombinant human growth hormone decreases lung and liver tissue lipid peroxidation and increases antioxidant activity after thermal injury in rats. J Burn Care Rehab. 1998;19:542-8.
- 10.Dagmar K, Schubert T, Horch ER, et al. Insulin treatment improves hepatic morphology and function through modulation of hepatic signals after severe trauma. Ann Surg. 2004;240:340-9.
- 11. Jeschke MG, Herndon DN, Barrow RE. Insulinlike growth factor I in combination with Insulinlike Growth Factor Binding Protein 3 affects the hepatic acute phase response and hepatic morphology in thermally ınjured rats. Ann Surg. 2000;231:408-16.
- 12. Friedman L, Chopra S, Grover S. Approach to the patient with abnormal liver biochemical and function tests. Up to date. April, 2014. Available at: https://www.uptodate.com/contents/liver-biochemical-tests-that-detect-injury-to-hepatocytes. Accessed June 30,2023.
- 13. Shinohara M, Kayashima K, Koomi K. Protective effects of verapamil on ischemia-induced hepatic damaged in the rat. Eur Surg Res. 1990;22:256-92.
- 14. Jeschke MG, Micak RP, Finnerty CC, et al. Changes in liver function and size after a severe thermal injury. Shock. 2007;28:172-7.
- 15. Livingston DH, Mosenthal AC, Deitch EA. Sepsis and multiple organ dysfunction syndrome: a clinical-mechanistic overview. New Horizons. 1995;3:276-87.
- 16. Nielson CB, Duethman NC, Howard JM, et al. Burns: Pathophysiology of Systemic Complications and Current Management. J Burn Care Res. 2017;38:469-81.
- 17.Holavanahalli RK, Helm PA, Kowalske KJ. Long-term outcomes in patients surviving large burns: the musculoskeletal system. J Burn Care Res. 2016;37:243-54.
- 18.Kılıç Ş, Sözüer EM, Deniz K, et al. Correlation of Serum Procalcitonin and Creatine Phospo-Kinase Levels with Tissue Histopathology in Rats Exposed to Experimental Electric Injury. Erciyes Med J. 2007;29:18-24.
- 19. Koop J, Loos B, Spilker G, et al. Correlation between serum creatinine kinase levels and extent of muscle damage in electrical burns. Burns. 2004;30:680-3.
- 20. Masanes MJ, Gourbiere E, Prudent J, et al. A high voltage electrical burn of lung parenchyma. Burns. 2000;26:659-63.
- 21. Yaşar MA, Yaşar D, Ramazan ÖD, ve ark. Yüksek voltaj elektrik çarpmasına bağlı akciğer ve karaciğer parankim yanığı. Fırat Tıp Dergisi. 2006;11:142-3.
- 22. Daniel R, Ballard A, Heroux P, et al. Highvoltage electrical injury: Acute pathophysiology. J Hand Surg. 1988;13:44-9.
- 23. Achauer B, Eriksson E, Guyuron B. Plastic Surgery Indications, Operations, and Outcomes. Ann Plast Surg. 2001;46:345.
Details
| Primary Language | Turkish |
|---|---|
| Subjects | Health Services and Systems (Other) |
| Journal Section | Research Articles |
| Authors | |
| Early Pub Date | July 28, 2023 |
| Publication Date | July 28, 2023 |
| Published in Issue | Year 2023 Volume: 4 Issue: 2 |
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