Malignant Hypertension with Encephalopathy: Symptoms, Diagnosis and Emergency Care Guidelines

Malignant Hypertension: Malignant hypertension includes both malignant hypertension and malignant hypertension. Malignant hypertension refers to a condition that progresses rapidly from the outset, or develops suddenly and rapidly after a slow progression over several years. It is common in young adults under 40 years old and the elderly, clinically manifesting as significantly elevated blood pressure, often consistently above 200/130 mmHg, and fundus examination may reveal retinal hemorrhage or exudates. Malignant hypertension is more common in young people, with diastolic blood pressure often exceeding 140 mmHg, and papilledema (grade II) presenting. Currently, it is believed that the pathological changes and clinical manifestations of the two are similar. If malignant hypertension is not treated promptly, it can rapidly transform into malignant hypertension. In other words, malignant hypertension is the most severe stage of malignant hypertension; therefore, they are currently collectively referred to as malignant malignant hypertension.

Early malignant hypertension may be asymptomatic or present only with headache, which is worse in the morning. It is often triggered by extreme fatigue, excessive mental stress, cold stimulation, or menopausal endocrine disorders, causing a sudden rise in blood pressure, with diastolic blood pressure exceeding 130 mmHg. Fundus examination may reveal retinal hemorrhage, exudates, or papilledema. Signs of heart failure may also appear, such as prominent apical impulse and cardiomegaly. However, renal impairment is the most prominent, often presenting with persistent proteinuria, hematuria, and casts in the urine. It may also be accompanied by intra-arterial hemolysis and disseminated intravascular coagulation, sometimes leading to hemolytic anemia, which often indicates a critical condition.

Malignant hypertension is a clinical emergency of hypertension. Although not as dangerous as hypertensive encephalopathy, it can be life-threatening if not treated promptly. Statistics show that the one-year survival rate is only 10%–20%, with most patients dying within one year. Those with no or mild renal impairment have a better prognosis and a possibility of long-term survival. The prognosis of malignant hypertension is related to its etiology, course, blood pressure level, fundus changes, and the degree of damage to the heart, brain, and kidneys. Patients with high blood pressure and severe damage to vital organs such as the heart, brain, and kidneys have a poorer prognosis. In recent years, due to in-depth research on malignant hypertension, improvements in treatment methods, and the emergence of new drugs, its prognosis has greatly improved.

Hypertensive encephalopathy: Hypertensive encephalopathy refers to a rapidly increasing blood pressure (generally diastolic pressure above 130 mmHg) leading to cerebral edema and increased intracranial pressure, causing a rapidly changing clinical syndrome. It commonly occurs in patients with malignant hypertension and a small number of patients with gradually progressive hypertension. It can also be seen in patients with acute glomerulonephritis, pregnancy-induced hypertension, renovascular hypertension, and pheochromocytoma. Clinically, it is mainly characterized by a sudden and rapid increase in blood pressure, headache, vomiting, irritability, convulsions, and altered consciousness. The headache is a diffuse, generalized headache, mainly in the forehead or occipital region, aggravated by coughing or exertion, and often accompanied by nausea and vomiting. Impaired consciousness is also common, ranging from mild lethargy, confusion, and drowsiness to severe coma, and may be accompanied by hemiplegia, hemianopsia, aphasia, and hemisensory disturbances. Seizures are another common symptom of hypertensive encephalopathy, manifesting as generalized or focal convulsions, which can lead to status epilepticus in severe cases. The convulsions occur due to focal necrosis of brain tissue and abnormal electrical discharges of cranial nerves under sustained intracranial hypertension.

Fundus examination in hypertensive encephalopathy may reveal papilledema or tortuous and thinning veins resembling silver threads, or arteriovenous crossings, and punctate hemorrhages in the retina. Lumbar puncture of cerebrospinal fluid may reveal increased pressure, increased protein content, or a small number of red and white blood cells. CT scans in hypertensive encephalopathy often show no abnormalities or only cerebral edema, which is one of the criteria for differentiating it from cerebral hemorrhage.

The pathogenesis of hypertensive encephalopathy is not yet fully understood, but most believe it is caused by a sudden and rapid increase in blood pressure, leading to a disruption of the autoregulation of cerebral arteries. Under normal circumstances, when blood pressure rises, cerebral arterioles constrict to prevent overfilling; when blood pressure drops, they dilate to ensure blood supply to the brain and maintain intracranial pressure within a normal range. However, when blood pressure rises sharply, this regulatory function is disrupted. The sustained and strong constriction of cerebral arterioles is followed by passive and forced dilation, leading to excessive cerebral perfusion and cerebral edema. This, in turn, increases intracranial pressure and produces a series of symptoms.

Hypertensive encephalopathy is a serious complication of hypertension. If not treated promptly, it often results in irreversible brain tissue damage due to persistently elevated intracranial pressure, or death due to brain herniation. Therefore, close monitoring of the patient's condition is crucial to prevent hypertensive encephalopathy. If it does occur, prompt and aggressive treatment is essential.