| disease | Acute Infectious Toxic Encephalopathy |
A syndrome characterized by the sudden onset of encephalitis-like clinical manifestations during the course (or stage of convalescence) of various acute infections and pestilential diseases (such as pneumonia, bacillary dysentery, influenza, diphtheria, whooping cough, scarlet fever, cold-damage disease, pyelonephritis, etc.). It is more common in adolescents and children. It is primarily the result of a toxic reaction of the human brain to the toxins of the aforementioned infections and pestilential diseases, as well as secondary cerebral hypoxia.
bubble_chart Clinical Manifestations
Sudden onset of cerebral symptoms such as high fever, headache, vomiting, dysphoria, delirious speech, aphasia, paralysis, and spasms often occurs during acute infections, pestilential diseases, or the stage of convalescence. Tendon reflexes may be hyperactive, weakened, or absent, with bilateral positive pathological reflexes. A few patients may exhibit cerebellar signs such as ocular tremor and ataxia. Severe cases may develop status epilepticus, decerebrate rigidity, or rapidly progress to unconsciousness, neck stiffness, dilated pupils, and sluggish or absent light reflexes. Mild cases often recover gradually within 1–2 days without any cerebral sequelae. A small number of critically ill patients may experience persistent high fever, unrelenting spasms, worsening consciousness impairment, and respiratory or circulatory failure, endangering their lives. Generally, the longer the cerebral symptoms persist, the greater the likelihood of sequelae.
1. It often occurs suddenly during the course of acute infections or pestilential diseases, or at the stage of convalescence, with symptoms such as high fever, headache, vomiting, dysphoria, delirious speech, aphasia, paralysis, and spasm. Tendon reflexes may be hyperactive, weakened, or absent, with bilateral pathological reflexes positive. A few patients may exhibit cerebellar signs such as ocular tremor and ataxia. Severe cases may develop status epilepticus, decerebrate rigidity, or rapidly progress to unconsciousness, neck stiffness, dilated pupils, and sluggish or absent light reflex. Mild cases often recover gradually within 1–2 days without any residual brain sequelae. A few critically ill patients may experience persistent high fever, unrelenting spasm, deepening consciousness impairment, and respiratory or circulatory failure, endangering their lives. Generally, the longer the brain damage symptoms persist, the greater the likelihood of sequelae.
2. Cerebrospinal fluid examination may show increased pressure and protein levels, normal glucose and chloride levels, and a grade I increase or normal white blood cell count, with no pathogenic bacteria detected in the cerebrospinal fluid.bubble_chart Treatment Measures
On the basis of actively treating the primary disease, strengthen treatments such as antispasmodic therapy (e.g., phenobarbital or phenytoin), antipyretic therapy (physical cooling, diaphoretic and antipyretic drugs), and anti-cerebral edema therapy (e.g., mannitol, furosemide). Pay attention to maintaining respiratory and circulatory functions, ensuring airway patency, nutrition, water-electrolyte metabolism, and acid-base balance. Additionally, administer appropriate doses of hormones and neurotrophic metabolic drugs as needed.
It should be differentiated from other central nervous system diseases such as encephalitis or meningitis.
