What is hypertensive encephalopathy?
Hypertensive encephalopathy is a group of clinical syndromes. The sudden increase of blood pressure caused by various reasons leads to severe headache, disturbance of consciousness, convulsions and various transient localized neurological symptoms, which is called hypertensive encephalopathy. The disease also belongs to the category of stroke. When the blood pressure is lowered rapidly, the condition can improve immediately.
Encephalopathy caused by malignant hypertension is the most common, followed by glomerulonephritis, gestational eclampsia, primary hypertension, pheochromocytoma, etc.
Previously, it was thought that hypertensive encephalopathy was cerebral vasospasm. In recent years, people realized that the disease was caused by the rupture of cerebral autoregulation function. Because of the rupture of cerebral autoregulation, increased cerebral blood flow, exudation, punctate hemorrhage, micro thrombus infarction and other pathological changes, the clinical symptoms of stroke can be caused.
Clinical symptoms of hypertensive encephalopathy?
Hypertensive encephalopathy showed stroke. Acute onset, all clinical symptoms peaked in 12-48 hours. The initial symptom is headache. It doesn’t start very early and gradually worsens, resulting in severe headache accompanied by jet vomiting. There is a disturbance of consciousness, which is manifested as confusion, nonsense, and continuous sleepiness, but it can respond to the call, and finally forms a coma. The above headache plus disturbance of consciousness is an indispensable and necessary symptom of hypertensive encephalopathy. In addition, there may also be some localized neurological symptoms, such as generalized or localized shaking, hemiplegia, stroke silence, etc.
The severe increase of arterial blood pressure is an important basis for the diagnosis of this disease. The average arterial pressure (divided by 2 after high pressure plus low pressure, that is, divided by 2 after systolic pressure plus diastolic pressure) is mostly between 150-200mmhg. Fundus examination showed fundus vasospasm, papilledema, retinal exudation and hemorrhage. EEG examination showed generalized or localized abnormalities. The above clinical manifestations will be significantly relieved after the blood pressure drops rapidly.
Hypertensive encephalopathy, cerebral embolism, cerebral hemorrhage and subarachnoid hemorrhage belong to the category of stroke. Although acute subdural hematoma and brain tumor are not stroke diseases, their symptoms have many similarities. Therefore, it is important to pay attention to the differential diagnosis in clinic to prevent misdiagnosis.
First of all, the speed of symptoms should be identified. The symptoms of hypertensive encephalopathy peak within 12-48 hours after the sharp rise of blood pressure. Cerebral thrombosis presents a slow onset, and all symptoms begin to appear in about 1-2 days. Cerebral vascular embolism presents acute onset. Hypertensive intracerebral hemorrhage develops symptoms within minutes to hours after onset. Subarachnoid hemorrhage has a rapid onset, and severe symptoms appear within minutes of onset. Acute subdural hematomas are all caused by trauma, and often show progressive deterioration within hours to days after trauma. The onset of brain tumors is slow, and symptoms can appear in a few days, weeks or months.
Secondly, the nature of headache is also somewhat different. Hypertensive encephalopathy presents with diffuse headache. There was no headache or little headache in cerebral infarction. Brain tumor is recurrent headache. Cerebral hemorrhage, subarachnoid hemorrhage and acute subdural hematoma all presented with severe headache.
Identify from the level of consciousness. Hypertensive encephalopathy has nonsense, blurred consciousness, and coma in severe cases. Cerebral embolism is mostly awake, with occasional mild lethargy, which can be responded by breathing. Hypertensive intracerebral hemorrhage worsened rapidly after the onset and quickly appeared in deep coma. Subarachnoid hemorrhage consciousness may be normal, or transient coma may occur. The degree of consciousness disturbance of acute subdural hematoma varies from mild to severe, and coma may occur after deterioration. Brain tumors are mostly awake without disturbance of consciousness.
Hypertensive encephalopathy how to grab the ball?
When hypertensive encephalopathy occurs clinically, the arterial blood pressure should be rapidly reduced, and as the blood pressure decreases, the symptoms can be immediately relieved. Drugs with good antihypertensive effect and rapid action, such as reserpine 1-2mg, can be used for intramuscular injection every 4-6 hours, or 60mg of nitroprusside can be added into 1000ml of 5% glucose, and the intravenous drip can be applied at the speed of 1-2ml / min. The effect can be achieved within 2 minutes after medication. At the same time, pay attention to reducing intracranial pressure, mannitol can be used for intravenous infusion, and oxygen inhalation, anticonvulsant and other treatment.
One notable study on hypertensive encephalopathy (HE) is “Hypertensive Encephalopathy: Clinical Features, Diagnosis, and Management” conducted by researchers from the Department of Neurology at the Mayo Clinic. This study aimed to provide a comprehensive overview of HE, including its clinical presentation, diagnostic criteria, and management strategies.
The primary focus of the study was to elucidate the clinical features of HE, a neurological syndrome that occurs as a result of severe and acute elevation of blood pressure, which can lead to cerebral edema, ischemia, and potentially fatal outcomes. The researchers discussed the typical manifestations, which include headache, confusion, seizures, and focal neurological deficits. They also explored the diagnostic process, which relies heavily on clinical assessment and neuroimaging techniques such as CT and MRI scans to identify characteristic patterns of brain swelling.
The study emphasized the critical importance of rapid blood pressure control in the management of HE to prevent further neurological damage and mortality. It recommended the use of intravenous antihypertensive medications, such as labetalol or nicardipine, to achieve and maintain blood pressure within a safe range. The researchers also highlighted the need for careful monitoring of renal function and electrolytes, as well as the potential role of mannitol in reducing intracranial pressure in severe cases.
This research contributed to the field by consolidating current understanding of HE and providing clear guidelines for clinicians on the prompt recognition and management of this acute and potentially devastating condition. It underscored the importance of a multidisciplinary approach, involving neurologists, nephrologists, and critical care specialists, to optimize patient outcomes. The study also stressed the need for further research to better understand the long-term neurological consequences and optimal therapeutic strategies in HE.
