![]() This syndrome generally develops after a lucid interval, and the most common symptoms are mental deterioration (amnesia, cognitive dysfunction), emotional disorders (depression, anxiety, mutism), urinary and faecal incontinence, and motor disorders (gait alterations, parkinsonian symptoms). This finding, normally undetectable in the acute phase of intoxication, is considered the cause of late-onset neuropsychiatric syndrome. Third, it may cause white matter demyelination. Cortical damage may manifest as transient vasogenic oedema or as a necrosis with infarct areas in the absence of cerebral artery occlusion. Second, although to a lesser extent, it may also cause focal lesions to the cerebral cortex, especially the hippocampus and temporal lobes. Firstly, CO directly causes diffuse hypoxic-ischaemic encephalopathy, which predominantly affects grey matter. There are 3 mechanisms by which CO damages the central nervous system. The clinical presentation and radiological findings of CO poisoning vary greatly. Three days later, hydrocephalus resolved and the external ventricular drain was removed after remaining closed for 48 hours without visible neurological deterioration. As of the fifth day after surgery, our patient's neurological symptoms had improved progressively, reaching an adequate level of consciousness and showing no focal neurological signs. Taken as a whole, these findings suggest multiple anoxic-ischaemic encephalic lesions secondary to CO poisoning. Patchy areas of small bilateral cortical infarcts could also be observed in the frontal and parietal lobes, as well as extensive infarcts in both cerebellar hemispheres, with the most damage occurring in the territory of the superior and anterior inferior cerebellar arteries no signs of hydrocephalus were seen. 2) showed multiple cerebral infarcts in an early subacute stage, extensively affecting the limbic system, hippocampus, fornix, and basal temporal area bilaterally. A follow-up cranial MRI scan performed 4 days after surgery ( Fig. After surgery, the patient remained in coma for the next 5 days (flexion–extension of both upper limbs was the only response to painful stimuli). The patient underwent emergency surgery: first, an external ventricular drain was put in place, from which exuded a clear liquid under high pressure, and then, a decompressive craniectomy of the posterior fossa was performed to relieve cerebellar herniation. 1) revealed severe hydrocephalus affecting the lateral ventricles and third ventricle, resulting in a significant mass effect. ![]() However, 72 hours after admission to the ICU, the patient's state of consciousness deteriorated suddenly. In the 48 hours after being admitted to the ICU, the patient's neurological symptoms improved to the point where he was able to obey simple instructions, although he remained drowsy. The patient was therefore mechanically ventilated with 100% oxygen until his carboxyhaemoglobin levels decreased to 0.9%, approximately 6 hours later. A urine toxicology test revealed benzodiazepine and methadone, while CO-oximetry showed carboxyhaemoglobin levels of 23.6%. The patient was admitted to the intensive care unit (ICU). 1) revealed diffuse hypodensities in both cerebellar hemispheres, basal temporal white matter bilaterally, both internal capsules, and the globus pallidus. Upon arrival at the emergency department, the patient had a low level of consciousness (Glasgow Coma Scale = 3) and mid-dilated miotic pupils which were poorly reactive as a result, he underwent orotracheal intubation. He was found unconscious inside a car inhaling exhaust gases, and beside him were 2 empty blister packs of benzodiazepines. He also presented personality disorder and had attempted suicide several times. The patient was a 38-year-old man with a medical history hypothyroidism treated with thyroid hormone replacement therapy. We present a case of CO poisoning in an adult male who developed acute obstructive hydrocephalus secondary to bilateral cerebellar oedema. ![]() The development of acute hydrocephalus is an extremely rare complication. Neurological sequelae constitute the principal cause of associated morbidity. This type of toxicity results from tissue hypoxia and CO-mediated damage at the cellular level. Carbon monoxide (CO) poisoning is one of the most common causes of morbidity and mortality by poisoning. ![]()
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