Internal and Emergency Medicine

, Volume 7, Supplement 1, pp 33–34

Early subcortical ischemic infarction and delayed leucoencephalopathy after carbon monoxide poisoning


  • Aftab Ahmad
    • Division of NeurologyNational University Hospital
    • Division of NeurologyNational University Hospital

DOI: 10.1007/s11739-011-0589-4

Cite this article as:
Ahmad, A. & Sharma, V.K. Intern Emerg Med (2012) 7: 33. doi:10.1007/s11739-011-0589-4

Carbon monoxide (CO) poisoning is a major cause of death following attempted suicide, as well as accidental and non-accidental exposures [1]. Although clinical presentation depends on the duration and the intensity of exposure, the assessment of the severity of intoxication is difficult, since most severely affected patients present in a comatose state. Presence of coma on arrival at the hospital generally indicates an extensive exposure. Consciousness is frequently regained after removal from the scene along with normobaric oxygen administration. A small percentage of patients, who show complete initial recovery may develop delayed neurological deficits, predominantly as neuropsychiatric and behavioral features.Neuroimaging findings in CO poisoning may result in early, as well as delayed changes. We describe the early and late clinical course and serial neuroimaging findings in a patient after CO poisoning.

A 42-year-old Chinese man was brought to the hospital after being found unconscious in his room filled with burning charcoal smoke. On arrival at the hospital, he was comatose (Glasgow coma scale 3 points) blood pressure 146/88 mmHg and carboxyhemoglobin level 30.9%. Drug screening for benzodiazepines, opiates and barbiturates was negative. He was intubated, and mechanically ventilated with 100% oxygen. Carboxyhemoglobin level decreased to 3.5% after 3 h, and to 0.5% after 12 h with an improved level of consciousness. Upon extubation the next day, he was orientated but noted to have a mild right-sided weakness. Further exploration revealed that he did not suffer from any chronic illness, and had burnt the charcoal in his room with suicidal intent.

Magnetic resonance imaging (MRI) of the brain revealed a left subcortical ischemic infarction (Fig 1a, 1b) with normal MRA (Fig 1c). Carotid duplex, and transthoracic echocardiography were unremarkable. He achieved complete functional recovery at 2 weeks after admission. Six weeks post hospitalization he became increasingly forgetful, and was slow in walking and talking. He was noted to have spasticity in all four limbs with bilateral upgoing Babinski signs, and some pseudobulbar features (emotional incongruity, dysphagia and brisk jaw jerk). A repeat brain MRI demonstrated symmetrical periventricular white matter hyperintensities (Fig 1d, 1e, 1f). Thyroid screen, connective tissue screen, nerve conduction studies and cerebrospinal fluid examination were within normal limits. His condition has remained unchanged during the past 12 months.
Fig. 1

Neuroimaging findings in carbon mono-oxide poisoning. Acute left subcortical ischemic infarction is noted on a brain MRI performed on day 2 (a, b). No intracranial stenosis was noted on MRA (c).Note the absence of significant white matter changes. Magnetic resonance imaging performed about 8 weeks later shows restricted diffusion in the subcortical white matter on axial T2 weighted (d), FLAIR (e) and diffusion-weighted sequences (f)

We report early and late clinical and neuroimaging manifestations in a patient with CO poisoning. The initial recovery was followed by a delayed neurological decline due to wide-spread leucoencephalopathy.

The MRI has great sensitivity for demonstrating the neuroimaging abnormalities due to CO poisoning, and changes may appear as early as 1-h post-exposure [2]. Acute CO poisoning characteristically shows deep gray involvement, most commonly of bilateral globus pallidii, thalami and putamen, with a hemorrhagic component [2]. Interestingly, our patient suffered from an acute left subcortical ischemic infarction, without any significant intracranial or extracranial arterial stenotic-occlusive disease.

Delayed neurological deterioration may occur in about 2.75% of the patients and individuals older than 50 years carry a greater risk [3]. Oligodendroglial injury is believed to be the underlying mechanism for demyelination in deeper subcortical structures. Patchy cortical necrosis, especially in hippocampi may also occur. Our patient was younger, but developed extensive delayed subcortical white matter changes.

Hyperbaric-oxygen therapy is often recommended for patients with acute carbon monoxide poisoning, especially in patients with severe poisoning and history of a loss of consciousness [4]. Hyperbaric-oxygen increases the dissolved oxygen content in the blood, and is believed to prevent lipid peroxidation in the brain [4]. However, it may be complicated by hyperoxic seizures and barotrauma. A randomized study of 76 patients demonstrates that the hyperbaric-oxygen therapy reduces the frequency of cognitive sequelae by 46% when assessed 6 weeks after symptomatic carbon monoxide poisoning [5]. Our center did not have the facilities for hyperbaric-oxygen therapy, and his comatose state prompted us to intubate him and to initiate mechanical ventilation, which resulted in a rapid reduction in his carboxyhemoglobin levels and improvement in the neurological status.

Our case serves as a reminder to the emergency physicians to institute hyperbaric-oxygen therapy in patients with severe carbon monoxide poisoning to prevent delayed neurological consequences. We feel that the imaging features described above, especially the delayed leucoencephalopathy, will appear and should be looked for especially if the delayed neuropsychiatric features appear in patients with history of a recent exposure to carbon monoxide.

Conflict of interest


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