Evaluation of Lung, Cardiac and Brain Pathologies of Death Cases Caused by Carbon Monoxide Poisoning

Research Article

Austin J Clin Neurol 2016; 3(1): 1085.

Evaluation of Lung, Cardiac and Brain Pathologies of Death Cases Caused by Carbon Monoxide Poisoning

Pehlivan S¹*, Alacam H², Samdanci E³, Kara D¹, Turkkan D¹, Altuntas A4, Gurler M² and Karapirli M5**

¹Department of Pathology- Morgue, Ankara Branch of the Council of Forensic Medicine, Turkey

²Department of Medical Biochemistry, Hacettepe University, Turkey

³Department of Pathology, Inonu University, Turkey

4Department of Chemistry, Ankara Branch of the Council of Forensic Medicine, Turkey

5Department of Forensic Medicine, Harran University, Turkey

*Corresponding author: Sultan Pehlivan, Department of Pathology - Morgue, Ankara Branch of the Council of Forensic Medicine, Ankara ŞefkatMah. Felek Cad. No: 45 Keçiören/Ankara 06300, Turkey

**Senior author: Mustafa Karapirli, Department of Forensic Medicine, School of Medicine, Harran University, Sanliurfa, Turkey

Received: April 14, 2016; Accepted: May 30, 2016; Published: June 02, 2016


Background: Carbon monoxide (CO) poisoning is a big problem and seen in the whole world. And, the pathological changes caused by CO poisoning is still investigated.

Aim: The aim of this study is to investigate the relationship between pathological changes and carboxyhemoglobin (COHb) levels.

Method: 127 death cases, due to CO poisoning, are included in the study. Lung tissue samples are examined histopathologically and evaluated in terms of edema, hemorrhage, congestion, pneumonia, bronchitis, emphysematous changes, foreign body aspiration and pleural pathology. Hemorrhage, edema and other specific findings in the brain are evaluated. For examination of cardiac tissue, secondary findings in the sectional myocardial ischemia and stenosis in the coronary artery sections are evaluated. And, the correlation between the pathological changes and COHb levels were investigated.

Results: Edema (80%), hemorrhage (27%), congestion (13%), emphysematous changes (42%), pneumonia (0.03%) and bronchitis (0.05%) were detected in the lungs. Cardiac pathologies such as coronary stenosis (11%), cardiac ischemia (0.007%) and fibrosis (0.08%) and brain lesions (0.03%) were located in the cases. However, no correlation between changes in cardiac and brain pathology with COHb levels were detected. A negative correlation was found between COHb with pneumonia and bronchitis.

Conclusions: As a result, besides damage in the central nervous system and heart, severe damage also occurs in the lungs and various clinical conditions such as edema, congestion and pneumonia can be seen. All these histopathologic findings may be helpful to consider planning of acute and long term treatment of CO poisoning.

Keywords: CO poisoning; Carboxyhemoglobin; Pulmonary edema; Pulmonary congestion


Carbon monoxide (CO) occurs from incomplete combustion of organic substances and it is a toxic gas with the features of colorless, odorless and non-irritating. CO is also formed during the destruction of the hem group in the human body and through the binding of hemoglobin (Hb), carboxyhemoglobin (COHb) arises. The COHb level in healthy individuals lies between 1-3%. But the COHb levels in the blood can reach up to 10-15% in persons that smoke a lot [1-4].

CO poisoning makes up nearly half of all deadly poisonings in the world [5,6]. Non-intentional CO poisoning takes place in different regions and different seasons in the world [7]. CO poisoning in Turkey is the most common cause of morbidity and mortality in the winter months. Also, considering all age groups, CO poisoning is the first reason of fatal poisonings in Turkey [8-11].

Pathological findings and clinical manifestations after CO poisoning depend on the CO exposure conditions. CO exposure can differ in amount and time. Short or long term exposure to high concentrations of gas or long term exposure to low concentrations of gas can cause CO poisoning [12].

CO shows its effect via hypoxia, cellular toxicity and free radicalmediated cellular injury. By binding itself to hemoglobin, CO slides the oxygen dissociation curve to the left which leads to less oxygen separating from the hemoglobin resulting in cellular hypoxia. Cellular toxicity arises through the connection of CO with different proteins and enzymes inside the cell. Especially, cytochrome c oxidase connected CO hinders the cells to use oxygen by the mitochondria. When electrons don’t reach the oxygen, they are separated from the carrier and cause free radical-mediated cellular injury inside the cell. An increase in lipid peroxidation resulting from the interaction of unsaturated fatty acids with oxygen free radicals after CO poisoning in rats [13,14].

During CO poisoning, depending on the impact level of hypoxia, different findings can arise. If the central nervous system is affected, headache, syncope, loss of consciousness varying from disorientation to coma, seizures, ataxia, behavioral disorders, dizziness, balance disorders and general weakness are observed. If the cardiovascular system is affected, palpitations, feeling of tightness in chest, cardiac arrhythmia and ischemic changes are especially seen in individuals with coronary artery diseases. Cardiorespiratory arrest can arise due to brainstem changes or severe cardiac hypoxia [15,16]. Besides the changes in the nervous and cardiac system, different levels of lung pathologies can also be observed. Pulmonary changes seen in CO poisoning are connected to prolonged hypoxia. These changes in the lungs are affected by the permeability of capillaries and cause edema [17,18]. Adult respiratory distress syndrome is rarely seen after CO poisoning [19]. Although all of these histopathological information’s related with CO poisoning in cardiac, lung and brain tissues, there are still some deficiencies in this area. Therefore, the aim of this study is to investigate the relationship between pathological changes in especially postmortem lung, heart and brain tissues and their COHb levels.

Materials and Methods

This is a retrospective study. Work permit was received by the Commission for Education and Scientific Research of the Forensic Medicine Institution (Date: March 12, 2013, number: B.03.1.ATK.


One hundred and twenty seven (127) death cases that resulted from CO poisoning, between the years of 2007 and 2012, were included in the study. Seventy (70) of those are men and 57 women. Demographic characteristics of the cases are shown in Table 1. Just, CO poisoning cases included in the study. The autopsies of the cases were conducted at the Institute of Forensic Medicine in the Morgue Department of the Ankara Group Presidency.