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Acute hydrocephalus in carbon monoxide poisoning
Author(s) -
Antón M,
Alcaraz A,
Rey C,
Concha A,
Fernández J
Publication year - 2000
Publication title -
acta paediatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.2000.tb18427.x
Subject(s) - globus pallidus , medicine , carbon monoxide poisoning , basal ganglia , white matter , magnetic resonance imaging , pathological , hydrocephalus , toxicity , anesthesia , pathology , hypoxia (environmental) , radiology , poison control , central nervous system , oxygen , chemistry , environmental health , organic chemistry
Carbon monoxide (CO) intoxication continues to be one of the most common causes of morbidity due to poisoning. The toxicity is caused by a combination of tissue hypoxia and direct CO‐mediated damage at the cellular level (1). Neurologic consequences of CO poisoning have been most often reported. Loss of consciousness, intermittent convulsions and respiratory failure may appear when carboxyhaemoglobin (COHb) concentrations of 60–80% are reached (2). However, it is important to recognize that COHb levels do not correlate with the severity of symptoms in a substantial number of cases (1). Pathological findings include necrosis and degeneration of the globus pallidus (3) and destructive lesions of the cerebral white matter (4). Computer tomography (CT) commonly shows bilateral low‐density areas in the globus pallidus (2–6) and low‐density lesions in the white matter (4). Magnetic resonance imaging (MRI) is more sensitive in detecting these lesions which appear as hyperintense signals in basal ganglia on T2 weighted images (4, 5). Neuropathological and radiological findings are well correlated (3).