CE - LETTER TO THE EDITOR

Early subcortical ischemic infarction and delayedleucoencephalopathy after carbon monoxide poisoning

Aftab Ahmad • Vijay K. Sharma

Received: 10 January 2011 / Accepted: 6 April 2011 / Published online: 16 April 2011

� SIMI 2011

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 fre-

quently 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 neuropsy-

chiatric 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 venti-

lated 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 transtho-

racic 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 periven-

tricular 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.

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 sub-

cortical ischemic infarction, without any significant intra-

cranial 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

A. Ahmad � V. K. Sharma (&)

Division of Neurology, National University Hospital,

Singapore 119074, Singapore

e-mail: drvijay@singnet.com.sg

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Intern Emerg Med (2012) 7 (Suppl 1):S33–S34

DOI 10.1007/s11739-011-0589-4

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 dis-

solved 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 cog-

nitive 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 improve-

ment in the neurological status.

Our case serves as a reminder to the emergency physi-

cians to institute hyperbaric-oxygen therapy in patients

with severe carbon monoxide poisoning to prevent delayed

neurological consequences. We feel that the imaging fea-

tures described above, especially the delayed leucoence-

phalopathy, 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 None.

References

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3. Gottfried JA, Mayer SA, Shungu DC, Chang Y, Duyn JH (1997)

Delayed post hypoxic demyelination. Association with arylsulfa-

tase A deficiency and lactic acidosis on proton MR spectroscopy.

Neurology 49:1400–1404

4. Piantadosi CA (1999) Diagnosis and treatment of carbon monox-

ide poisoning. Respir Care Clin N Am 5:183–202

5. Weaver LK, Hopkins RO, Chan KJ et al (2002) Hyperbaric oxygen

for acute carbon monoxide poisoning. N Engl J Med 347:

1057–1067

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)

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