Hidayatullah Hamidi1, Mohammad Tahir Aien1
1Department of Radiology, French medical institute for children (FMIC), Kabul, Afghanistan.
Corresponding Author: Hidayatullah Hamidi, Department of Radiology, French medical institute for children (FMIC), Kabul, Afghanistan, Tel: 0093 744 733 605; E-Mail:Hidayatullah.email@example.com
Received Date: 16 Apr 2016
Accepted Date: 05 Jul 2016
Published Date: 07 Jul 2016
Copyright © 2016 Hamidi H
Citation: Hamidi H and Aien MT. (2016). CT Features of Carbon Monoxide Poisoning Induced Brain Ischemic Changes. Mathews J Case Rep 1(3): 011.
Carbon monoxide poisoning can cause serious damage to brain and myocardium. The sites more commonly affected in the brain are globus Pallidus, caudate nucleus, putamen, thalamus and cerebral white matter. The authors present a case of Carbon Monoxide poisoning in a 33 year old previously healthy electrician who was exposed unintentionally to generator smoke in a close environment for approximately one hour and the patient was unconscious thereafter. Nonenhanced brain Computed tomography was performed on the third day of exposure and revealed diffuse white matter ischemic changes and brain edema.
Non enhanced axial CT sections were taken through the head with 128 slice Siemens scanner. Diffuse white matter hypodensities were noted in bilateral cerebral hemispheres (Figure 1).
Figure 1: Non enhanced axial CT section: Diffuse white matter hypo-densities are noted in bilateral cerebral hemispheres.
Altered corticomedulary differentiation was also noted with features of brain edema evident by effacement of anterior horns of bilateral lateral ventricles and cortical sulci. (Figure 2)
Figure 2: Non enhanced axial CT section: altered corticomedullary differentiation with effaced anterior horns of bilateral lateral ventricles. The cortical sulci are also effaced due to diffuse brain edema.
Bilateral middle cerebral arteries appeared denser in these non-enhanced CT images, most probably secondary to adjacent parenchymal low attenuation as a result of ischemia and edema. (Figure 3)
Figure 3: Non enhanced axial CT images: The middle cerebral arteries (MCA) are dense. The right MCA is well seen in right image and the left MCA in left image.
Carbon monoxide (CO) is a lethal, toxic gas produced by incomplete burning of carbon-based fuels and substances . Intoxication occurs by inhalation of natural gas, smoke or automobile exhaust . CO poisoning can cause serious (acute and delayed) damage to brain and myocardium . Various mechanisms are described responsible for brain damage, the most important being hypoxia .
AREAS AFFECTED IN BRAIN
The diagnosis is usually suggested clinically .
Signs and symptoms are directly proportional to the level of CO in blood. At lower levels; headache is the commonest symptom, while at higher levels, mental status changes, dyspnea, and syncope may occur. Very high levels of intoxication can result in myocardial ischemia, ventricular arrhythmias, pulmonary edema, lactic acidosis, seizures, hypotension, coma, and death .
While the diagnosis is usually made clinically and treatment should be started, imaging is useful for understanding pathophysiologic mechanism, delineation of disease extent and determining the prognosis [1, 2, 11].
CT is usually the first line, rapid imaging modality while MRI can depict the changes more precisely, especially in areas where CT is of limited value; like hippocampus .
The main imaging features are those of ischemic insult (hypodensity in CT, low signal on T1WI, high on T2WI and FLAIR images and diffusion restriction) .
Management depends on early diagnosis and initiation of hyperbaric oxygen therapy, as treatment is of benefit in reversing both cerebral and myocardial tissue damage .
Based on severity of insult, the prognosis differs from complete recovery, to long-term neurologic sequelae, and even death [2, 10].
Lesions within deep WM are indicator of a poor prognosis and absence of white matter changes at follow up CT suggest likely improvement .