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Delayed Encephalopathy after Acute Carbon Monoxide Poisoning with Dynamic Progression of Radiologic and Clinical Manifestations

Author(s): Shuang-Shuang Song, Ying Li, Lei Niu, Song Liu, Chong-Feng Duan, Qing-Lan Sui, Ji-Ping Zhao, Yan-De Ren, Xue-Jun Liu


To analyze retrospectively one case of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) that demonstrated both clinical and radiological progression and to summarize the experiences learned from the treatment of this case.


Radiologic and clinical data from this case of DEACMP were reviewed.


This patient had a normal C-reactive protein (CRP) level but an increased D-dimer level upon admission. A MRI scan of the brain indicated abnormal signals in the left thalamus and right centrum semiovale, along with mild abnormal signals in the bilateral symmetrical globus pallidus lesions (unfortunately, this sign was overlooked). He was initially diagnosed with cerebral infarction according to radiologic findings. After admission, the patient underwent symptomatic treatment and reexamination, and a routine blood test revealed an increased CRP level and a decreased D-dimer level. MRI scan revealed enlargement of the lesion in the right centrum semiovale, as well as new lesions in the bilateral parietal and occipital lobes. Based on clinical manifestations, a preliminary diagnosis of autoimmune encephalitis was made, and the patient’s conditions improved after symptomatic treatment. However, the symptoms were aggravated after lowering the hormone dose. Then he had another MRI scan, which revealed symmetrical signal abnormalities in the basal ganglia regions bilaterally and white matter around the posterior and anterior horns of lateral ventricles bilaterally. A normal CRP level was basically restored per a routine blood test, and the D-dimer level increased to 3580 ng/ml. According to clinical and radiological process, radiologist inquired the patient’s history, he admitted to having an explicit history of CO exposure. Therefore, the patient was finally diagnosed with DEACMP.


Early MRI findings of DEACMP may include atypical and asymmetric white matter lesions. Moreover, the signal abnormalities of the bilateral symmetrical globus pallidus lesions are not pronounced in the subacute stage and, therefore, may be easily neglected. Cerebral infarction may precede any white matter lesions. Laboratory tests including serum CRP and D-dimer levels can aid in the diagnosis of DEACMP.

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