The Clinical Association Between Carbon Monoxide Poisoning and Troponin I levels 1 BS ;
Tiffany Sahadeo Gary Tackling Rohun Gupta Tashina Dussie Viliane 2 2 2 2 1,2 Villcant MD ; Mirette Atnas MS ; Demian Omeh MD ; Ofek Hai DO ; Roman Zeltser MD ; 1,2 and Amgad N. Makaryus MD 1Donald
2 MD ;
1 BS ;
2 MD ;
and Barbara Zucker School of Medicine at Hofstra/Northwell 2Nassau University Medical Center NY, USA
Background Carbon monoxide (CO) has a 230 times higher affinity for hemoglobin than oxygen. When carbon monoxide is introduced into the body, it binds to hemoglobin, forming carboxyhemoglobin. Carbon monoxide outcompetes oxygen and causes oxygen saturation of hemoglobin to decrease, leading to a reduction of oxygen delivery and tissue hypoxia. The organ systems that are most sensitive to hypoxia are those with a large oxygen demand, such as heart. This can result in myocardial injury, as evidenced by a “leak” in troponins, electrocardiogram changes, and myocardial necrosis. In clinical practice, carbon monoxide poisoning is commonly encountered. It is responsible for over 50,000 estimated visits to the Emergency department as well as approximately 1200 deaths per year. Although there is a high prevalence, there is insufficient data that examines the association between laboratory biomarkers and clinical outcomes. This study will investigate the association between troponin levels and its effect on clinical outcomes in carbon monoxide poisoning.
Hypothesis
• Myocardial injury was found in 22/119 or 18.5% of patients • Mean troponin level was 0.755 ± 3.03 mg/ml. • Myocardial injury was associated with higher in-hospital mortality OR 21.33 (p=0.008) • Older age was associated with higher in-hospital mortality OR 1.08 (p=0.03) • When adjusted for age, the association of myocardial injury with higher mortality remained statistically significant OR 21.37 (p=0.01) • No statistically significant difference was found with respect to age, comorbidities, gender, race, and ethnicity in pts with and without myocardial injury Total number of patients
119
Demographics
58.8% male 64.7% White 21.0% Black 5.0% Asian 9.2% Hispanic
Co-morbidities
The hypothesis is that carbon monoxide-induced cardiac injury as evidenced by elevated troponin levels may adversely affect clinical outcomes, such as higher rates of Intensive Care Unit admission, intubation and in-hospital mortality.
This study is based on a retrospective chart review of 119 patients evaluated for carbon monoxide exposure between the dates of January 1st, 2012 and August 31, 2019 The demographic information was gathered from the EMR. All evaluated patients were over the age of 18 years and assessed for pre-existing cardiovascular risk factors such as comorbidities (HTN, CAD, HF) and smoking status. The patients were classified based on the presence or absence of myocardial injury via serum troponin ≥0.5mg/mL (positive troponin level) to decipher if a correlation exists between myocardial injury and ICU admission and in-hospital mortality. SSPS analytic software was used for data analysis.
Overall outcomes intubated in-hospital mortality Mean LOS
19.3% 4.2% 5.2 ± 14.2 days
Daniel Satran, Christopher R. Henry, Cheryl Adkinson, Caren I. Nicholson, Yiscah Bracha, Timothy D. Henry. Cardiovascular Manifestations of Moderate to Severe Carbon Monoxide Poisoning. Journal of the American College of Cardiology May 2005, 45 (9) 1513-1516; DOI: 10.1016/j.jacc.2005.01.044 Hajsadeghi S, Tavakkoli N, Jafarian Kerman SR, Shahabadi A, Khojand M. Electrocardiographic Findings and Serum Troponin I in Carbon Monoxide Poisoned Patients. Acta Med Iran. 50(3):185-191
MI
Non-MI
P=0.002
20
P=0.009
10 0
ICU admission
Future Directions
Cha YS, Cha KC, Kim OH, et al. Features and predictors of myocardial injury in carbon monoxide poisoned patients Emerg Med J 2014;31:210-215.
40 30
3. Older age is another independent factor that increases in-hospital mortality.
Resources
Additional Clinical Outcomes 50
2. No statistically significant difference was found with respect to age, comorbidities, gender, race, and ethnicity in patients with and without myocardial injury.
The information collected can assist in the creation of protocols for physicians to treat the cardiac injury induced by carbon monoxide when a patient presents to the hospital with carbon monoxide poisoning.
37% Hypertension 21% Diabetes 17.6% Hyperlipidemia 11.8% CAD 5% CHF 4.2% Atrial Fibrillation 4.2% COPD 5.9% Asthma 21% Smoking History
60
1. Myocardial injury induced by carbon monoxide exposure adversely impacts clinical outcomes. There is a positive association between myocardial injury as defined by elevated troponin levels and increased ICU admission, intubation as well as in-hospital mortality.
4. This information is important in providing care for patients with carbon monoxide poisoning and in determining the cardiac effects of such an exposure.
Table 1: Patient demographics and overall outcomes
Percentage
Methods
Summary
Results
Intubation
Figure 1: Comparison of rates of intubation and ICU admission in patients with and without myocardial injury
Huysal K, Ustundag Budak Y, Aydin U, Demirci H, Turk T, Karadag M. COHb Level and High-Sensitivity Cardiac Troponin T in 2012 in Bursa, Turkey: A Retrospective SingleCenter Study. Iran Red Crescent Med J. 2016;18(5):e27061. Published 2016 Feb 20.doi:10.5812/ircmj.27061 Henry C, Satran D, Lindgren B, Adkinson C, Nicholson C, Henry T. Myocardial Injury and Long-Term Mortality Following Moderate to Severe Carbon Monoxide Poisoning. JAMA January 2006, 295 (4) 398-402 Montagnana M, Lippi G. Troponin elevation reflects myocardial injury in carbon monoxide poisoning. Biochimica clinica 2013, 37 (3): 246-249 Yurtseven S, Arslan A, Eryigit U, et al. Analysis of patients presenting to the emergency department with carbon monoxide intoxication. Turk J Emerg Med. 2016;15(4):159–162. Published 2016 Mar 8. doi:10.1016/j.tjem.2015.05.001