Carbon Monoxide Intoxication Treatment in Intensive Care; Retrospective Analysis of the Cases

Yıl 2020, Cilt: 42 Sayı: 1, 39 - 47, 01.01.2020

Gülçin Aydın , İşın Gençay , Selim Çolak , Burak Aktan Ünase Büyükkoçak

https://doi.org/10.20515/otd.459264

Öz

In this study, we
aimed to determine the etiological and demographic characteristics of patients
with carbon monoxide intoxication to reveal their relationship with the
clinical findings, and to investigate the treatment processes and prognoses of
these patients. A total of 63 patients diagnosed with carbon monoxide intoxication
and hospitalized in the Department of Anesthesiology and Reanimation Intensive
Care Unit between 2014 and 2017. The age avarage of the patients was 44.9 years.
32 patients were female and 31 patients were male. The avarage duration between
exposion and reffering to emergency department was 6.22 hours. Initial COHb
value avarage was 27%. Most common exposion to carbonmonoxide was 61,9% winter
and common source of exposion was 93,7% heating stove. Avarage GCS at emergency
admission was 14.1. Neuropsychiatric symptoms were observed in 79.4%,
gastointestinal symptoms were observed in 36.5%, respiratory symptoms were
observed in 15.9% and cardiovascular symptıms were observed in 11.1% of the
patients. Two patients required 
mechanical ventilation, 57 patients required noinvasive mechanical
ventilation (NIMV) and 12 patients required hyperbaric oxygen (HBO) treatment.
The avarage of GCS at discharge was 15. Hospital stay duration avarage was 1.71
days. Patients were divided into three groups according to their COHb levels at
admission, COHb levels under 10% mild (Group 1), between 11-25% intermediate
(Group 2), between 26-45% serious (Group 3) and over 41% very serious (Group
4). There were statistically significant difference between groups in means of pH
levels, admission GCS, otologic symptoms, NIMV requirement, SpO2 levels and CK,
CK-MB levels. Patient were also divided into two groups according to their GCS
scores at admission, Group A (GCS=15) and Group B (<15). There were
statistically significant difference between groups in means of COHb levels at
admission, cardiovascular symptoms, presence of comorbidities, respiratory
symptoms, HBO requirement, CK and troponin levels and mechanical ventilation
requirement. Patients who had HBO treatment (Group I) and who had not
hyperbaric oxygen treatment (Group II) were comperatively evaluated. Troponin-I
(p=0,015) , CK (P=0,032) levels and mechanical ventilation requirement
(p=0,003) were significantly higher but GCS scores (p<0,001) were
significantly lower at Group I. At the same time a significant positive
corelation between HBO treatment requirement and troponin,CK levels was found.
As a result, management of the patients that diagnosed as carbon monoxide
intoxication along with GCS scores at admission, COHb, CK,CK-MB and lactate
levels is very important effects on prognosis and treatment of the patients.

Anahtar Kelimeler

Carbon monoxide intoxication, carboxyhemoglobin

Karbonmonoksit İntoksikasyon Tanısı ile Yoğunbakımda Tedavi Edilen Olguların Analizi

Öz

Bu çalışmanın amacı
karbon monoksit intoksikasyon tanılı hastaların etyolojik ve demografik
özelliklerini belirlerken, klinik bulguların tedavi sürecine ve prognoza
etkisini araştırmaktır. Çalışmaya 2014-2017 yılları arasında Yoğun Bakım
Ünitemizde karbon monoksit intoksikasyon tanısı ile yatan 63 hasta dahil
edildi. Yaş ortalaması 44.49 yıl olan hastaların 32’si kadın, 31’i erkek idi.
Maruziyet sonrası acil servise başvuru süresi ortalama 6.22 saat idi. Başvuru
anında COHb değeri ortalama %27 idi. En sık maruziyet %61.9 ile kış mevsiminde
iken en sık maruziyet kaynağı %93.7 ile soba idi. Acil servise başvuru anında
ortalama GKS puanı 14.1 puan idi. Hastaların %79.4’ünde nöropsikiyatrik
semptomlar, %36.5’inde gastrointestinal semptomlar, %23.8’inde solunum sistemi
semptomları, %15.9’unda otolojik semptomlar, %11.1’inde ise kardiyovasküler semptomlar
vardı. İki hastada mekanik ventilatör, 57 hastada noninvazif mekanik ventilatör
(NIMV) ve 12 hastada hiperbarik oksijen tedavisi ihtiyacı oldu. Hastaların
çıkış GKS değerleri ortalama 15 idi. Hastanede ortalama yatış süreleri 1.71 gün
idi. Hastalar başvuru anındaki COHb düzeylerine göre; COHb düzeyi %10’nun
altında hafif (grup 1), %11-25 arası orta (grup 2), %26-40 arası ağır (grup 3),
%41 üzeri çok ağır (grup 4) olarak gruplandırıldı. Gruplar arasında pH, GKS
geliş puanı, otolojik semptomlar, NIMV ihtiyacı, SpO2, CK-CKMB düzeyi değerleri
arasında istatistiksel olarak anlamlı fark bulundu. Hastalar hastaneye başvuru
anındaki GKS puanlarına göre grup A (GKS=15) ve grup B (GKS<15) olarak
sınıflandırıldı. gruplar arasında; COHb geliş düzeyi, KVS semptomlar, ek
hastalık varlığı, solunum sistemi semptomları, mekanik ventilatör ihtiyacı, HBO
ihtiyacı, CK ve troponin düzeyi açısından istatistiki olarak anlamlı fark
vardı. Hiperbarik oksijen tedavisi alan (grup I) ve almayan (grup II) hastalar
da karşılaştırmalı olarak değerlendirildi. grup I’de troponin-I (p=0.015),
CK(p=0.032) düzeylerinde ve mekanik ventilasyon ihtiyacında (p=0.003) belirgin
artış olduğu, GKS’nun düşük olduğu (p<0.001) tespit edildi. Bununla birlikte
HBO tedavisi gereksinimi ile troponin ve CK seviyesi arasında pozitif yönde
korelasyon olduğu görüldü. Bu çalışma sonunda karbon monoksit intoksikasyon
tanılı hastalarda başvuru anındaki GKS puanı, COHb, CK-CKMB ve laktat
değerlerinin klinik bulgular ile birlikte yorumlanmasının hem tedavi hem de
prognoz üzerinde önemli etkilerinin olabileceği düşünüldü.

Anahtar Kelimeler

Karbonmonoksit intoksikasyonu, karboksihemoglobin, hiperbarik oksijen tedavisi

Kaynakça

• 1. Partrick M, Fiesseler F, Shih R, Riggs R, Hung O: Monthly variations in the diagnosis of carbon monoxide exposures in the emergency department. Undersea & Hyperbaric Medicine 2009, 36(3):161.
• 2. Kandis H, Katırcı Y, Çakır Z, Aslan Ş, Uzkeser M, Bilir Ö: Acil servise karbon monoksit entoksikasyonu ile başvuran olguların geriye dönük analizi. Akademik Acil Tıp Dergisi 2007, 5:21-25.
• 3. Elif D, Akgür SA, Oztürk P, Sen F: Fatal poisonings in the Aegean region of Turkey. Veterinary and human toxicology 2003, 45(2):106-108.
• 4. Salameh S, Amitai Y, Antopolsky M, Rott D, Stalnicowicz R: Carbon monoxide poisoning in Jerusalem: Epidemiology and risk factors. Clinical toxicology 2009, 47(2):137-141.
• 5. İnal V: Karbonmonoksit Zehirlenmesi ve Tedavisi. Turkiye Klinikleri Journal of Anesthesiology Reanimation 2005, 3(1):34-41.
• 6. Lapresle J, Fardeau M: The central nervous system and carbon monoxide poisoning II. Anatomical study of brain lesions following intoxication with carbon monoxide (22 cases). Progress in brain research 1967, 24:31-74.
• 7. Keles A, Demircan A, Kurtoglu G: Carbon monoxide poisoning: how many patients do we miss? European Journal of Emergency Medicine 2008, 15(3):154-157.
• 8. Hampson NB, Hauff NM: Carboxyhemoglobin levels in carbon monoxide poisoning: do they correlate with the clinical picture? The American journal of emergency medicine 2008, 26(6):665-669.
• 9. Chan MY, Au T, Leung KS, Yan WW: Acute carbon monoxide poisoning in a regional hospital in Hong Kong: historical cohort study. Hong Kong medical journal 2016, 22(1):46-55.
• 10. Salluh JI, Soares M: ICU severity of illness scores: APACHE, SAPS and MPM. Current opinion in critical care 2014, 20(5):557-565.
• 11. Satar S. Acilde Klinik Toksikoloji. Nobel Kitabevi Adana 2009.
• 12. Satran D, Henry CR, Adkinson C, Nicholson CI, Bracha Y, Henry TD: Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. Journal of the American College of Cardiology 2005, 45(9):1513-1516.
• 13. Moon JM, Shin MH, Chun BJ: The value of initial lactate in patients with carbon monoxide intoxication: in the emergency department. Human & experimental toxicology 2011, 30(8):836-843.
• 14. Benaissa ML, Megarbane B, Borron SW, Baud FJ: Is elevated plasma lactate a useful marker in the evaluation of pure carbon monoxide poisoning? Intensive care medicine 2003, 29(8):1372-1375.
• 15. Marchi AG, Renier S, Messi G, Barbone F: Childhood poisoning: a population study in Trieste, Italy, 1975-1994. Journal of clinical epidemiology 1998, 51(8):687-695.
• 16. Teksam O, Gumus P, Bayrakci B, Erdogan I, Kale G: Acute cardiac effects of carbon monoxide poisoning in children. European Journal of Emergency Medicine 2010, 17(4):192-196.
• 17. Yelken B, Tanrıverdi B, Çetinbaş F, Memiş D, Süt N: The assessment of QT intervals in acute carbon monoxide poisoning. Anatolian Journal of Cardiology/Anadolu Kardiyoloji Dergisi 2009, 9(5).
• 18. Aslan S, Erol MK, Karcioglu O, Meral M, Cakir Z, Katirci Y: The investigation of ischemic myocardial damage in patients with carbon monoxide poisoning. The Anatolian journal of cardiology 2005, 5(3):189-193.
• 19. Dogan NO, Savrun A, Levent S, Gunaydin GP, Celik GK, Akkucuk H, Cevik Y: Can initial lactate levels predict the severity of unintentional carbon monoxide poisoning? Human & experimental toxicology 2015, 34(3):324-329.
• 20. Icme F, Kozaci N, Ay M, Avci A, Gumusay U, Yilmaz M, Satar S: The relationship between blood lactate, carboxy-hemoglobin and clinical status in CO poisoning. Eur Rev Med Pharmacol Sci 2014, 18(3):393-397.
• 21. Şen H: Karbonmonoksit Zehirlenmesi. TAF Preventive Medicine Bulletin 2009, 8(4):351-356.
• 22. İncekaya Y, Feyizi H, Bayraktar S, Ali İ, Topuz C, Karacalar S, Turgut N Karbonmonoksit Zehirlenmesi ve Hiperbarik Oksijen Tedavisi Okmeydanı Tıp Dergisi 33(2):114-118, 2017
• 23. Kandiş H, Katırcı Y, Karapolat B: Karbonmonoksit zehirlenmesi. Düzce Üniversitesi Tıp Fakültesi Dergisi 2009, 11(3):54-60.
• 24. Prockop LD, Chichkova RI: Carbon monoxide intoxication: an updated review. Journal of the neurological sciences 2007, 262(1):122-130.
• 25. Hampson NB, Piantadosi CA, Thom SR, Weaver LK: Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning. American journal of respiratory and critical care medicine 2012, 186(11):1095-1101.