Sodium loss coma is a loss of sodium due to gastrointestinal disorders, surgery, and infection that can precipitate a crisis as in primary hyperaldosteronism. Peripheral circulatory collapse is particularly pronounced in this type of critical coma. It is important to note that increased sodium excretion may occur during the first few days of corticosteroid administration, probably because the glomerular filtration rate, which was low, is increased after treatment. It has been reported that less than 1 week after treatment with corticosteroids, patients enter a coma with a significant negative sodium balance. In addition, when thyroid preparations are applied alone, especially when the dosage is too large, the metabolic rate increases and the body’s need for adrenocorticotropic hormone increases, making the lack of adrenocorticotropic hormone more serious. Sodium loss coma occurs suddenly, sometimes as a result of a blow to the head, or as a result of an extracranial lesion. Of course, the degree of sodium loss coma varies from one cause to another, but sodium loss coma caused by pathological factors should be taken seriously and should be seen by a hospital in time to avoid spreading the disease. Causes of sodium loss coma: 1, brain blood circulation disorders and insufficient essential nutrients The normal function of the brain depends on the normal flow of blood carrying oxygen and glucose to provide sufficient energy for brain metabolism. When the cerebral perfusion pressure drops to a certain level, ischemic damage to brain tissue occurs within a few minutes, and if the circulation stops, the patient can lose consciousness within 15 seconds. More than 5 minutes can cause permanent brain damage. 2, endogenous metabolic disorders People in the occurrence of serious damage to important organ function or acute serious infection, will produce some toxic metabolites, they can cross the blood-brain barrier, inhibit the brainstem reticular structure and cerebral cortex function, triggering sodium loss coma. For example, the occurrence of hepatic encephalopathy is related to many metabolites and toxic substances. 3.Exogenous poisoning Certain drugs or poisons can easily inhibit the reticular structure of brainstem. Especially sedative-hypnotics and anesthetics, most of them have selective inhibition on synaptic transmission of brainstem reticular structures. Sodium loss coma can occur with excessive ingestion. Some toxins cause sodium loss coma by inhibiting some important enzyme systems in the body (e.g. organophosphorus compounds mainly inhibit cholinesterase, etc.).