YAHYA KEMAL GÜNAYDIN, Kubilay VURAL, Mehtap OK AKÇİL, Yvuz KATIRCI, Dilber KOCAŞABAN ÜÇÜZ, YAVUZ YİĞİT, FİGEN ÇOŞKUN

Comparison of carbon monoxide poisonings originated from coal stove and natural gas and the evaluation of Neutrophil/Lymphocyte ratio

Amaç: Bizim çalışmamızdaki amacımız ülkemizde karbonmo- noksit (CO) zehirlenmesinin en sık nedeni olan kömür sobasın- dan kaynaklanan zehirlenmeler ile doğal gaz kaçaklarının yol açtığı zehirlenmeler arasındaki epidemiyolojik, klinik, laboratu- ar ve prognoz farklılıklarını ortaya koymaktır. Ayrıca CO zehir- lenmelerinde oluşan klinik tablonun şiddeti, prognozu, kompli- kasyonları ile başvuru sırasındaki nötrofil/lenfosit oranı ( NLO ) arasındaki ilişkiyi incelemeyi amaçladık. Yöntemler: Bu prospektif çalışmaya Ankara Eğitim ve Araş- tırma Hastanesi Acil Tıp Kliniğine 2009 Ekim 2010 Nisan tarihleri arasında başvuran akut karbonmonoksit zehirlenmesi olgularının tümü alındı. CO zehirlenmesi tanısı, anemnezinde CO zehirlenmesine neden olabilecek öykünün olması ile birlikte karboksihemoglobin (COHb) konsantrasyonunun % 10nun üs- tünde olması şeklinde konuldu. Çalışmamıza toplam 100 hasta dahil edildi. Bulgular: 55 (%55) hasta kömür sobasıyla zehirlenirken, 45 (%45) hasta doğal gaz kaynaklı zehirlenmişti. Doğal gazdan zehirlenen grubun ortalama COHb düzeyi anlamlı bir şekilde daha yüksekti (p=0,01). Doğal gaz grubunun ortalama Glas- kow koma skoru (GKS) değeri anlamlı bir şekilde daha düşüktü (p=0,018). Doğal gazdan zehirlenen grupta 17 hastanın HBO (hiperbarik oksi jen) tedavisi ihtiyacı olurken, kömür sobasından zehirlenen grupta ise sadece 6 hastanın HBO tedavisi ihtiyacı oldu. Doğal gazdan zehirlenen grupta kömür sobasından ze- hirlenen gruba göre anlamlı bir şekilde HBO tedavisi ihtiyacı daha fazlaydı. (p=0,001) NLO ile COHb oranı, troponin ve GKS değerleri arasında istatistiki olarak anlamlı bir ilişki bulunmadı (Sırasıyla; p=0,872, p=0,470, p=0,896). Sonuç: Doğal gaz kaynaklı CO zehirlenmeleri kömür sobası zehirlenmelerine göre daha toksik olabilmektedir. CO zehirlen- melerinde oluşan klinik tablonun şiddeti, prognozu, komplikas- yonları ile başvuru sırasındaki NLO arasında her hangi bir ilişki yoktur.

Kömür sobası ve doğal gaz kaynaklı karbonmonoksit zehirlenmelerinin karşılaştırılması ve Nötrofil/Lenfosit oranının değerlendirilmesi

Objective: The aim of our study is to present the epi- demiologic, clinical, laboratory and prognosis differences between the coal stove origin poisoning and natural gas leakages. We also aimed to investigate relationship be- tween the severity of clinical picture, prognosis, complica- tions develop in CO poisoning with neutrophil/lymphocyte ratio (NLR) at the initial admission. Methods: All the acute carbon monoxide cases who ap- plied to Ankara Training and Research Hospital Emergen- cy Medicine Clinic between October 2009 and April 2010 were included to this prospective study. CO poisoning diagnosis was made by the history of CO poisoning with carboxyl hemoglobin (COHb) concentration is over 10%. 100 patients were included to our study. Results: Of the patients, 55(55%) were poisoned from the coal-stove and 45(45%) from natural gas leakage. The mean COHb level of the natural gas group was sig- nificantly high (p=0.01). The mean value of GCS of the natural gas group was significantly lower (p=0.018). The number of patients with indication for HBO therapy were 17 and 6 in the natural gas group and coal-stove group, respectively, being significantly higher in the natural gas group(p=0.001). There was no statistically significant re- lationship between the value of NLR and values of COHb, troponin, and GCS (p=0.872, p=0.470, and p=0.896, re- spectively). Conclusions: Carbon monoxide poisoning from natural gas leakage is more toxic than that from the coal-stove. There is no relationship between NLR at the time of pre- sentation and the severity of clinical findings, prognosis and complications

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1. Raub JA, Mathiue-Nolf M, Hampson NB, et al. Carbon mon- oxide poisoning-a public health perspective. Toxicology 2000;145:1-14. 2. Turan M.İ, Çayır A, Olgun H. Delayed encephalopathy after acute carbon monoxide poisoning. Dicle Med J 2014;41:217-218. 3. Omaye ST. Metabolic modulation of carbon monoxide toxic- ity. Toxicology 2002;180:139-150. 4. Abelsohn A, Sanborn MD, Jessiman BJ, et al. Identifying and managing adverse environmental health effects: 6. Carbon monoxide poisoning. CMAJ 2002;166:1685-1690. 5. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med 1998;339:1603-1606. 6. Turner M, Hamilton-Farrell MR, Clark RJ. Carbon monoxide poisoning: an update. J Accid Emerg Med 1999;16:92-96. 7. Raphael JC, Elkharrat D, Jars-Guincestre MC, et al. Trial of normobaric and hyperbaric oxygen for acute carbon mon- oxide intoxication. Lancet 1989;2:414-419. 8. İnal V. Carbon monoxide poisoning and treatment. Turkiye Klinikleri J Anest Reanim 2005;3:34-41. 9. Choi IS. Carbon monoxide poisoning: systemic manifesta- tions and complications. J Korean Med Sci 2001;16:253- 261. 10. Handa PK, Tai DY. Carbon monoxide poisoning: a five year review at Tan Tock Seng Hospital, Singapore. Ann Acad Med Singapore. 2005;34:611-614. 11. Horne BD, Anderson JL, John JM, et al. Which white blood cell subtypes predict increased cardiovascular risk? J Am Coll Cardiol 2005;45:1638-1643. 12. Núñez J, Núñez E, Bodí V, et al. Usefulness of the neutro- phil to lymphocyte ratio in predicting long-term mortality in ST segment elevation myocardial infarction. Am J Car- diol 2008;101:747-752. 13. Macrez R, Ali C, Toutirais O, et al. Stroke and the immune system: from pathophysiology to new therapeutic strate- gies. Lancet Neurol 2011;10:471-480. 14. Nagai M, Terao S, Yilmaz G, et al. Roles of inflammation and the activated protein C pathway in the brain edema associated with cerebral venous sinus thrombosis. Stroke 2010;41:147-152. 15. Kamisli S, Kamisli O, Gonullu S, et al. The prognostic val- ue of increased leukocyte and neutrophil counts in the early phase of cerebral venous sinus thrombosis. Turk J Cerebro- vasc Dis 2012 18:2;39-42. 16. Hampson NB, Mathieu D, Piantadosi CA, et al. Carbon monoxide poisoning: interpretation of randomized clinical trials and unresolved treatment issues. Undersea Hyperb Med 2001;28:157-164. 17. Brvar M, Mozina H, Osredkar J, et al. S100B protein in carbon monoxide poisoning: a pilot study. Resuscitation 2004;61:357-360. 18. Kyne L, Hausdorff JM, Knight E, et al. Neutrophilia and congestive heart failure after acute myocardial infarction. Am Heart J 2000;139:94-100. 19. Gazi E, Bayram B. Relationship between Neutrophil/Lym- phocyte ratio and complications in patients with acute myo- cardial infarction. Anatol J Clin Invest 2012;6:17-20. 20. Yardan T, Cevik Y, Donderici O. et al. Elevated serum S100B protein and neuron-specific enolase levels in carbon monoxide poisoning. Am J Emerg Med 2009;27:838842. 21. Ertaş G, Sönmez O, Turfan M. et al. Neutrophil/lympho- cyte ratio is associated with thromboembolic stroke in patients with non-valvular atrial fibrillation. J Neurol Sci 2013;324:49-52