Carbon monoxide poisoning
Citation, DOI and article data
Carbon monoxide (CO) poisoning may result in an anoxic-ischemic encephalopathy, with acute as well as delayed effects.
Carbon monoxide poisoning is mostly preventable with common causes including malfunctioning heating systems, improperly ventilated motor vehicles, and residential fires 9. It is also observed as an attempt to commit suicide.
Patients can present with 10:
- acute symptoms of headache, dizziness, altered conscious state, seizures
- chronic symptoms of cognitive decline, abnormal gait, fecal incontinence
The pathophysiology can be two-fold:
- carbon monoxide strongly binds to hemoglobin and the resultant carboxyhemoglobin in the bloodstream can cause profound hypoxic/anoxic injury
- carbon monoxide is also a respiratory chain metabolism toxin that interferes with mitochondrial oxidative phosphorylation and activates polymorphonuclear leukocytes, which undergo diapedesis and cause brain lipid peroxidation; this results in the delayed effects of carbon monoxide poisoning
Changes tend to be bilateral with the globus pallidus most commonly affected 2.
Classically seen as low attenuation in the globus pallidus region. Other features include diffuse hypoattenuation in cerebral white matter 4.
Regions of involvement are similar to CT. Signal characteristics include:
- T1: affected areas are usually low signal, hemorrhagic areas can be high signal
- T2/FLAIR: affected areas are high signal
- T1 C+ (Gd): can show patchy peripheral enhancement in affected areas in the acute phase 2
- DWI: affected areas show increased diffusion signal in the acute phase
Treatment and prognosis
Treatment consists of administering 100% oxygen which accelerates the elimination of carboxyhemoglobin 9.
For involvement in and around the globus pallidus, consider:
- mitochondrial encephalopathies: tends to affect other basal ganglia regions
- other toxic encephalopathies
- other causes of anoxia
- metabolic disorders
- prion encephalopathies
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