Nasal myiasis is a rare parasitic disease. The growth of myiasis in the nasal cavity causes damage to the nasal cavity and paranasal sinuses. Once the dipeterous larvae are migrated, it causes damage to the surrounding structures such as eyes and skull cavity. Proper treatment and active prevention and control can reduce and avoid the occurrence of serious complications. On May 14, 2020, a patient with cerebral infarction and coma was admitted to Xiangya Hospital of Central South University and developed nasal myiasis. During the treatment of the primary disease, the patient was found to be infected with rhinomyiasis. The patient was treated with dehydration, cranial pressure reduction, brain protection, blood glucose control, blood pressure control, and anti-infection. Nasal endoscopy and nasal irrigation were carried out to treat nasal myiasis. The patient was properly placed and isolated for prevention and control so as to prevent the spread of myiasis in the ward. After 16 days, the patient regained consciousness, no worm was found in the nasal cavity, and was discharged from the hospital. The patient was followed-up for 6 months, no maggots were found in the nasal cavity of the patients, no complaints of nasal discomfort was occurred, and no other patients and medical staff were infected with myiasis. The prevention of myiasis is very important, and proper measures should be taken to reduce the risk of community and hospital infection.
鼻蝇蛆病是一种较为罕见的寄生虫病，蝇蛆在鼻腔内生长对鼻腔、鼻窦造成损伤，一旦移行，会导致眼、颅腔等周围结构受损，妥善治疗和积极防控才能减少和避免严重并发症的出现。2020年5月14日中南大学湘雅医院收治的1例脑梗死昏迷患者发生了鼻蝇蛆病。该患者在治疗原发病的过程中，发现感染了蝇蛆。给予脱水降颅压、护脑、控制血糖和血压、抗感染等，积极治疗原发疾病，对鼻腔进行了鼻内镜检查/取虫、鼻腔冲洗等以治疗鼻蝇蛆病，然后对患者进行了妥善安置和隔离防控，以防止蝇蛆病在病区内播散。入院第16天后，患者神志恢复，鼻腔内未再发现虫体，病情好转出院。随访6个月，患者鼻腔未再发现蝇蛆，未诉鼻腔不适，收治病区无患者及医务人员感染蝇蛆。蝇蛆病重在预防，应当积极采取措施以降低社区及医院感染的风险。.

Cortical blindness induced by hepatic encephalopathy is an extremely rare complication and its epidemiology has not been studied in great detail. We report a 63-year-old man with liver cirrhosis who developed sudden bilateral visual impairment.
On arrival at hospital, the patient had orientation disturbance, slurred speech, and mild disturbance of consciousness with impaired vision (light sense). He had no focal neurological deficits except for bilateral blindness. Cerebral stroke was suspected, but imaging and ophthalmological examination did not reveal major abnormalities. An increased concentration of ammonia in blood suggested hepatic encephalopathy; a diagnosis of cortical blindness was proposed. His vision returned gradually with relief of hepatic encephalopathy.
Cortical blindness can be an initial symptom of hepatic encephalopathy without severe disturbance of consciousness, and can be misdiagnosed as cerebral stroke. Cortical blindness induced by hepatic encephalopathy has been reported in only 10 cases, including our patient, and merits further evaluation.