Ischemic-hypoxic encephalopathy is commonly seen in conditions such as carbon monoxide poisoning, As syndrome, allergic reactions, and anesthesia accidents, and is clinically manifested by impaired consciousness, limb movement disorders, and cognitive impairment. Delayed ischemic-hypoxic encephalopathy is a secondary brain damage that is aggravated again after improvement of the primary ischemic-hypoxic symptoms and signs. The pathophysiological mechanism is not well understood and may be related to abnormalities in brain sulfate enzyme metabolism. What could be the reason for delayed ischemic-hypoxic encephalopathy, which is clinically more common in carbon monoxide toxic encephalopathy and less common in patients surviving through As syndrome, allergic reaction and anesthesia accident? I think the possible reasons are: patients with carbon monoxide poisoning can recover better after acute hyperbaric oxygen treatment, so the symptoms of delayed brain damage can be shown again, while patients with ischemic-hypoxic encephalopathy caused by As syndrome, allergic reactions and anesthesia accidents show severe impairment of consciousness clinically, so even if the symptoms of delayed encephalopathy appear later, they may not be able to show up and are masked by the symptoms of severe impairment of consciousness. The patient’s severe impaired consciousness symptoms are masked.