Carbon monoxide (CO) poisoning

Clinical History

A 25-year-old male patient came to our attention in state of unconsciousness (GCS 4/15). PA 50/70, 100 bpm, O2 saturation: 98%

Imaging Findings

After stabilisation of vital signs, the patient underwent a CT scan of the brain. CT reported poor representation of subarachnoid spaces, without any significant alteration of parenchymal density (Fig. 1). 24 hours later a brain MR was performed, thus showing the presence of a large bilateral area of restricted diffusivity within deep white matter, corona radiata and corpus callosum. In addition, other two spots of restricted diffusivity were visible within globus pallidus bilaterally (Fig. 3). All the described areas were hyperintense on T2 WI and FLAIR (Fig. 2), isointense on T1, and did not show contrast enhancement (Fig. 4).
Imaging findings were compatible with anoxic-ischaemic encephalopathy. Further clinical findings confirmed carbon monoxide poisoning.

Discussion

CO intoxication is one of the main causes of death by poisoning and was first described by Claude Bernard, who identified CO as the cause of hypoxia due to strong interaction with Hbg. CO is a colourless, odourless and tasteless gas that has 210x higher affinity to Hbg than for O2, thus leading to erythrocytes’ disability to transport oxygen. Direct consequences of CO poisoning are hypoxia, reduced cellular oxygen metabolism, lipid peroxidation and oxidative injury. The neuropathological consequence is demyelination and necrosis of deep white matter, necrotic lesions in globus pallidus (GP), hippocampus, cortex and cerebellum, with saving of U fibers (Grinker mielinopathy). [1, 2]
The clinical presentation is characterised by acute toxicity, presenting as nausea, headache, cognitive impairment, loss of consciousness, seizure and coma. Neurological sequelae are dementia, memory deficits, personality disturbance, parkinsonian-like symptoms [1].
Computed Tomography is usually negative; sometimes symmetric hypodensity in GP and diffuse hypodensity in cerebral WM can be described.
MR is a useful imaging technique, and is frequently positive at early stage of poisoning. At this stage, MR usually shows bilateral T2 hyperintensities of GP surrounded by hypointense rim and confluent T2 hyperintensity of deep white matter bilaterally and centrum semiovale, as result from diffuse demyelination. Grandient echo sequences can depict diffuse microhaemorrhages. All these areas are usually hyperintense on Diffusion Weighted Images, with low ADC values, due to restricted diffusion caused by cytotoxic oedema [3]. After contrast medium administration, T1W1 may show enhancement in GP, often in patient with acute poisoning.
In chronic phase, T2 hyperintensity become more evident within corpus callosum, subcortical U-fibers, internal and external capsules, and low signal can be reported in thalamus and putamen, due to iron deposition. Furthermore, in chronic stage a gradual increase of ADC values is described [2, 3].
Treatement of choice for CO poisoning consists in hyperbaric oxygen therapy, which has to be made within six hours. Early administration of 100% oxygen or HBO may prevent long-term neuropsychiatric sequelae.

Differential Diagnosis List

Final Diagnosis

Carbon monoxide poisoning

URL:	https://www.eurorad.org/case/10981
DOI:	10.1594/EURORAD/CASE.10981
ISSN:	1563-4086