carbon monoxide poisoning

Carbon monoxide (CO) poisoning may result in an anoxic-ischemic encephalopathy, with acute as well as delayed effects.

Epidemiology

Carbon monoxide poisoning is mostly preventable with common causes including malfunctioning heating systems, improperly ventilated motor vehicles, and residential fires . It is also observed as an attempt to commit suicide.

Clinical presentation

Patients can present with :

• acute symptoms of headache, dizziness, altered conscious state, seizures
  • cardiac arrest may occur, see pulseless electrical activity (PEA)
• chronic symptoms of cognitive decline, abnormal gait, fecal incontinence

Pathology

The pathophysiology can be two fold:

• carbon monoxide strongly binds to hemoglobin and the resultant carboxyhemoglobinin 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

Radiographic features

Changes tend to be bilateral with the globus pallidus most commonly affected .

CT

Classically seen as low attenuation in the globus pallidus region. Other features include diffuse hypoattenuation in cerebral white matter .

MRI

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
• 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 .

Differential diagnosis

For involvement in and around the globus pallidus, consider:

• mitochondrial encephalopathies: tends to affect other basal ganglia regions
  • Leigh disease
  • Kearns-Sayre syndrome
• other toxic encephalopathies
  • cyanide neurotoxicity: tends to also affect the cortex
  • methanol neurotoxicity: tends to affect the putamen
  • organophosphate neurotoxicity
• other causes of anoxia
• metabolic disorders
  • Wilson disease
• prion encephalopathies
  • Creutzfeldt-Jakob disease

Siehe auch:

• hypoxischer Hirnschaden
• T2 hyperintense Basalganglien
• Globus pallidus
• Morbus Wilson
• Leigh-Syndrom
• Creutzfeldt-Jakob-Krankheit
• Kearns-Sayre-Syndrom
• toxische Enzephalopathie

und weiter:

• Basalganglienverkalkungen
• ADC abnormality of the basal ganglia
• neuroradiologisches Curriculum
• respiratory chain metabolic toxins
• Chorea Huntington
• carbon monoxide