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Decoding hypertensive encephalopathy: Why are its symptoms so severe?
Hypertensive Encephalopathy (HE) is a brain dysfunction caused by high blood pressure. Symptoms of this condition include headache, nausea, difficulty with balance, and confusion, and often come on quickly. In addition to these more common symptoms, complications such as seizures, posterior reversible encephalopathy syndrome, and fundus hemorrhage may result. Hypertensive encephalopathy usually has blood pressure values above 200/130 mmHg, but sometimes occurs as low as 160/100 mmHg. However, diagnosis of this condition requires ruling out other possible causes.
Hypertensive encephalopathy is a rare but serious condition that often affects patients who have limited access to medical care.
Symptoms and their severity
Hypertensive encephalopathy is most common in young and middle-aged hypertensive patients. Although a certain percentage of patients with hypertension will develop this disease, its overall incidence is still quite low. It has been reported that from 0.5% to 15% of patients with malignant hypertension will develop hypertensive encephalopathy. Over the past few decades, advances in the detection and treatment of high blood pressure have led to a gradual decline in the condition's incidence. Symptoms usually appear within 12 to 48 hours after a sudden and sustained increase in blood pressure. The first symptom is a severe headache, which occurs in more than 75% of patients.
After experiencing a headache, patients may feel uneasy and may experience confusion and memory impairment within a few hours.
If left untreated, these neurological symptoms may worsen and eventually lead to coma. Other more serious symptoms include irritability, nausea, blurred images, seizures, and twitching of the limbs. Vision changes, including blurred vision, hemifield defects, and color blindness, are common in about a quarter of patients.
Cause and pathological mechanism
The cause of hypertensive encephalopathy is a sharp increase in blood pressure, which may be caused by acute nephritis, maternal epilepsy, chronic hypertensive crisis, and sudden discontinuation of antihypertensive drugs. In addition, conditions such as pheochromocytoma, Cushing's disease, and renal artery thrombosis can also cause this disease. Cerebral blood flow impairment caused by hypertensive encephalopathy remains controversial. Cerebral blood flow is usually maintained through self-regulatory mechanisms, but this mechanism fails when hypertension is excessive. When arterial blood pressure rises rapidly, cerebral blood vessels may spasm, leading to hypoxia and cell edema.
Cerebral edema can be classified as widespread or localized, and may cause compression of the ventricles and cortex, resulting in delayed vision and consciousness.
Diagnostic methods
The diagnosis of hypertensive encephalopathy requires physical examination, blood pressure measurement, blood tests, electrocardiogram, electroencephalogram, chest X-ray, urinalysis and head imaging examination. Because controlling blood pressure is critical, antihypertensive medications are often administered pending laboratory test results. Electroencephalography can be used to detect disorders of consciousness.
Treatment Overview
The initial treatment goal of a hypertensive crisis is to rapidly reduce diastolic blood pressure to approximately 100 to 105 mmHg, which should usually be achieved within two to six hours, with a maximum initial reduction of no more than 25% of overall blood pressure. This blood pressure control target will help gradually treat necrotizing vasculopathy; overly aggressive antihypertensive treatment may lead to other complications, such as ischemic events. Pharmacological treatment usually begins with intravenous antihypertensive drugs, such as sodium nitroprusside or labedol, which produce rapid therapeutic effects.
Prognosis
If treated promptly, patients with hypertensive encephalopathy usually recover without sequelae. But without timely intervention, the disease can lead to death. Historically, descriptions of this condition date back to the early 20th century, and were first described by Oppenheimer and Fishberg in 1928.
Although our understanding of hypertensive encephalopathy is increasing, many questions remain to be answered about how this condition can be identified and treated more effectively earlier.
