hypertensive encephalopathy



Overview

  • An acute brain injury caused by sudden and severe hypertension.
  • The main manifestations are headache, convulsions, blindness, impaired consciousness, and may be accompanied by transient hemiparesis, aphasia, and other focal neurologic symptoms.
  • Caused by various reasons of severe hypertension
  • The main treatment is blood pressure control, elimination of cerebral edema, antiepileptic drugs, etc.
  • Definition

  • Hypertensive encephalopathy is an acute cerebral syndrome caused by sudden, severe hypertension, in which the patient’s mean arterial pressure can be greater than 150 mmHg (normal is about 90 mmHg).
  • It is mainly related to extensive vasospasm of small cerebral arteries, which causes cerebral edema, capillary rupture and tissue necrosis due to cerebral ischemia and hypoxia.
  • Morbidity

  • The prevalence of hypertension in adults aged 18 and above in China is about 27.9%, and the number of hypertensive patients is about 244.5 million.
  • Hypertensive encephalopathy can occur at any age and is most common in patients aged 20 to 40.
  • The incidence of hypertensive encephalopathy in patients with essential hypertension is about 1%.
  • Questions you may be concerned about

    What is the difference between hypertensive encephalopathy and hypertensive crisis?

    The difference between hypertensive encephalopathy and hypertensive crisis is the different pathogenesis, symptoms, etc. Hypertensive encephalopathy and hypertensive crisis are not the same disease. It is recommended to take medication on time and test your blood pressure regularly.

    1. Pathogenesis: The pathogenesis of hypertensive encephalopathy is the increase of intracranial pressure and cerebral blood vessels caused by the dilation of small arteries in the brain, and even cerebral hernia; however, hypertensive crisis is due to the temporary spasm of small arteries all over the body, which leads to the obstacle of cerebral blood circulation.

    2. Symptoms: patients with hypertensive encephalopathy will have convulsions, coma and other symptoms; patients with hypertensive crisis will have dizziness, nausea, blurred vision and other symptoms, and may even cause pulmonary edema, angina and other symptoms.

    The appearance of these two diseases are generally caused by hypertension is not well controlled, it is recommended to pay attention to their own high blood pressure status in normal times. If you are not feeling well, you should go to the hospital for examination and treatment in time.

    Causes

    Causes

  • Hypertensive encephalopathy is mainly related to primary hypertension, secondary hypertension, and carotid endovascular treatment.
  • The incidence of hypertensive encephalopathy in primary hypertension is about 1%, and it is more likely to occur in people with longer history of hypertension and obvious cerebral vascular sclerosis.
  • Secondary hypertension, such as glomerulonephritic hypertension, renal artery stenosis, pheochromocytoma, and hypertensive syndrome of pregnancy also have the potential to develop hypertensive encephalopathy. The risk of hypertensive encephalopathy is especially high in the most severe stage of hypertensive disease in pregnancy (eclampsia).
  • Hypertensive encephalopathy, or hyperperfusion syndrome, can also be caused by a sudden increase in cerebral perfusion after carotid endarterectomy or stenting in patients with high carotid artery stenosis.
  • Predisposing factors

    Hypertensive encephalopathy may also be triggered by drugs or food.

    Drugs that may induce hypertensive encephalopathy

  • Hypertensive encephalopathy can be triggered by the use of monoamine oxidase inhibitors (MAOIs) in combination with rohypnolines, methyldopa, or postganglionic sympathomimetic agents in hypertensive patients.
  • Common MAOI drugs: isoniazid, furazolidone, ketoconazole, ashwagandha, eugenol (bactrim hydrochloride), phenelzine, bromfenacil, toloxanone, isoxazolidine, phencyclidine, moclobemide, selegiline, and methylbenzylhydrazine.
  • Postganglionic sympathetic depressants: quetiapine, pentamethylguanidinium tartrate, etc.
  • Foods that may induce hypertensive encephalopathy

    Hypertensive encephalopathy can also be induced by eating amine-rich foods, such as pickles, bacon, sausages, over-smoked foods, fried and battered foods.

    Pathogenesis

  • The average arterial pressure in healthy adults is about 90 mmHg, with an autoregulatory range between 60 and 150 mmHg. The rate and degree of elevation of blood pressure is the most important factor in determining the occurrence of hypertensive encephalopathy.
  • Under normal conditions, blood pressure rises and the small cerebral arteries diastole to ensure blood supply to the brain and keep intracranial pressure within normal limits. However, when the blood pressure rises sharply, the cerebrovascular autoregulation is dysfunctional, the small cerebral arteries undergo sustained and strong contraction followed by passive diastole, cerebral edema occurs due to over-perfusion of the brain, and the intracranial pressure rises and produces a series of symptoms.
  • When blood pressure rises sharply, extensive fibrin deposition (fibrin-like necrosis) exists throughout the middle and small arteries of the brain. Hypertensive encephalopathy occurs in patients with chronic hypertension, and changes such as arterial intimal atrophy, hyperplasia, hyaline-like changes, tiny infarcts, and tiny aneurysms can also be found.
  • Symptoms

    Main Symptoms

  • The typical manifestations of hypertensive encephalopathy are headache, convulsions, impaired consciousness, and a sharp rise in blood pressure, which can often exceed 220/120 mm Hg.
  • Headache often starts sharply, mostly in the whole head or occipital pain.
  • As the headache worsens, it may be accompanied by vomiting.
  • Blurred vision, restlessness, drowsiness or even coma.
  • There may be transient dark dawn, hemiparesis, aphasia and other manifestations.
  • In some patients, seizures are often characterized by convulsions of the limbs, upward glances of the eyes and loss of consciousness, or there may be different manifestations such as convulsions of some limbs, frothing, and immobility of the eyes.
  • In addition, blurred vision, vision loss, fundus changes, left ventricular enlargement, cardiopulmonary dysfunction and other signs may occur.
  • Complications

    Cerebral edema/brain hernia

  • Mostly caused by extensive cerebral vasogenic edema.
  • Early symptoms are headache, nausea, vomiting, drowsiness or unresponsiveness. In severe cases, irregular or sudden respiratory arrest and coma may occur.
  • Renal impairment, renal failure

  • Hypertension secondary to kidney disease or excessively high blood pressure can exacerbate or cause kidney function damage and kidney failure.
  • Symptoms such as oliguria, back pain, hematuria, and facial edema may occur.
  • Visual impairment

    Patients may develop optic papillary edema and occipital lobe infarction, causing blurred vision, vision loss and even blindness (cortical blindness).

    Cardiovascular infarction

    Some patients may cause myocardial infarction and cerebral infarction, manifesting as palpitations, chest tightness, chest pain, persistent limb paralysis, aphasia and other symptoms.

    Consultation

    Department of Medicine

    Emergency Department

    If there are symptoms such as elevated blood pressure, acute headache, seizures, impaired consciousness, loss of vision, etc., it is recommended to call the 120 emergency number or send the patient to the Emergency Department for emergency treatment.

    Neurology

    If you have symptoms such as headache, limb weakness, blackout, aphasia, etc., it is recommended that you go to the Department of Neurology for prompt medical treatment.

    Preparation

    Preparation for medical consultation: registration, preparation of information, common problems

    Tips for seeking medical treatment

  • Try to record the symptoms and duration of the onset of the disease so that you can give your doctor more information.
  • The patient’s condition develops rapidly and he/she has difficulty in moving around, so it is recommended that family members accompany him/her to the doctor and avoid driving or riding to the doctor by yourself.
  • Preparation Checklist

    Symptom list

    Particular attention should be paid to the time of onset of symptoms, special manifestations, etc.

  • Is there a history of hypertension? What is the highest blood pressure? How is it normally controlled and how well is it controlled?
  • Is there nausea, dizziness, darkness before the eyes?
  • Is there any limb weakness, unsteady walking, decreased sensation, numbness, etc.?
  • Any headaches? What is the degree? What is the nature? How long did it last?
  • Have similar symptoms occurred before?
  • List of medical history
  • Is there hypertension?
  • Was it during pregnancy and did hypertension develop during pregnancy?
  • What medications were taken prior to onset? What foods were eaten?
  • Checklist

    Test results of the last six months, which can be carried to the doctor’s office

  • Imaging examination: head CT examination, head magnetic resonance examination MRI.
  • Blood pressure examination: routine blood pressure examination, 24-hour ambulatory blood pressure examination.
  • Medication list

    Medication used in the last 3 months, if there is a medicine box or package, you can bring it to the doctor

  • Antihypertensive drugs: nifedipine, valsartan, amlodipine, etc.
  • MAOI medications: isoniazid, furazolidone, ketoconazole, ashwagandha, eugenol (bactrim hydrochloride), phenelzine, bromfenacilimine, toloxazone, isoniazid, phencyclidine, moclobemide, selegiline, methylbenzylhydrazine, and others.
  • Postganglionic sympathetic depressants: quetiapine, pentamethylguanidinium tartrate, etc.
  • Diagnosis

    Diagnosis is based on

    Medical history

    The patient may have a history of hypertension, renal disease, hypertensive syndrome of pregnancy, or other causes of high blood pressure.

    Clinical manifestations

    Symptoms
  • High blood pressure often reaches 180/120 mmHg or mean arterial pressure reaches 150 mmHg or more.
  • Acute headache, seizures, impaired consciousness, blackouts, hemiparesis, and aphasia may be present.
  • These symptoms may resolve rapidly as blood pressure-lowering treatments become effective.
  • Physical Signs

    The doctor will check for abnormalities in vital signs, movement, sensation, swallowing, tendon reflexes, and pathologic reflexes.

  • Vital signs: Check for normal, stable blood pressure, heart rate, pulse, pupils, and breathing.
  • Ophthalmologic examination: check whether the visual acuity and field of vision are normal.
  • Motor function examination: Observe whether the patient can complete movements such as closing the eyes, puffing out the cheeks, raising the eyebrows, etc.; observe whether the patient can complete movements such as lifting the hands, sitting up, standing, walking, etc., and whether he/she needs assistance.
  • Skin sensory examination: use a cotton swab to slide on the patient’s skin or use a blunt needle to gently prick the skin to assess the degree of sensory impairment based on the sensitivity to sensation; observe the patient’s response to hot and cold objects to assess the degree of temperature sensory impairment.
  • Pathological reflex examination: use percussion hammer to strike the periosteum and tendons, use blunt bamboo stick to gently stroke the corresponding parts of the forearm, sole of the foot, dorsum of the foot, etc., to check whether the muscle and tendon reflexes are abnormal.
  • Fundus examination

  • The fundus of the eye is visualized through fundoscopy.
  • Patients with this disease may show papillary edema, retinopathy hemorrhage, exudation, retinal artery spasm and other manifestations.
  • Imaging

  • Commonly used tests: magnetic resonance imaging (MRI) scanning and enhancement of the head, CT scanning and enhancement of the head.
  • Typical manifestations include diffuse cerebral edema in the subcortical white matter of both cerebral hemispheres, which is basically symmetrically distributed, especially in the parieto-occipital lobes, with shallow sulci, narrowed longitudinal fissure pools, and varying degrees of ventricular size on both sides of the brain.
  • In rare cases, the lesion area may be asymmetrically distributed, occurring in the basal ganglia, cerebellum and brainstem, and combined with hemorrhage.
  • Enhanced scans show no or mild enhancement of the lesion area. The lesion is completely absorbed after treatment.
  • Cerebrospinal fluid examination

  • Cerebrospinal fluid (CSF) can be used to help determine the cause of symptoms based on changes in white blood cell and protein levels in the cerebrospinal fluid.
  • Typical changes are increased cerebrospinal fluid pressure and increased protein content.
  • Differential Diagnosis

    Stroke

  • Similarities: patients may have a history of high blood pressure, and both may have sudden onset of headache, nausea, vomiting, confusion, seizures, or coma.
  • Differences:
  • Clinical symptoms are difficult to distinguish, mainly through cranial MRI, CT and other examinations.
  • Stroke patients may have clear hemorrhage and infarction lesions, and cerebral edema is relatively mild.
  • Viral encephalitis

  • Similarity: may have sudden headache, nausea, vomiting, convulsions, impaired consciousness and other symptoms.
  • Differences:
  • Viral encephalitis is usually accompanied by fever, stiff neck, and may have a generalized rash. Recent exposure to patients with viral encephalitis, history of viral infection or mosquito bites. There is mostly no history of hypertension and no severe elevation of blood pressure after the onset of the disease.
  • Cranial MRI shows that the lesions mostly involve the frontotemporal lobe of the cerebral cortex, and the symptoms of epilepsy are more prominent and recalcitrant, with specific manifestations on EEG and cerebrospinal fluid laboratory tests.
  • Venous sinus thrombosis

  • Similarity: usually present with intractable headache, accompanied by nausea, dizziness, vomiting and other symptoms in severe cases.
  • Differences:
  • Patients with venous sinus thrombosis may have no history of hypertension and no severe elevation of blood pressure after the onset of the disease, and funduscopic examination is mostly unremarkable.
  • Cranial MRI examination may show that the lesion mostly involves bilateral parieto-occipital cortex, paracentral lobules, and may be accompanied by cerebral infarction or hemorrhage.MRA examination may show stenosis, filling defects, and occlusion of the deep and shallow veins of the intracranial veins and venous sinuses.
  • Treatment

  • Treatment aim: rapid and smooth reduction of blood pressure, improvement of symptoms and prevention of complications.
  • Treatment principle: based on supportive therapy, use medication to lower blood pressure, reduce cerebral edema, and antiepileptic drugs.
  • Supportive treatment

  • Bed rest, close monitoring of consciousness, pupil, pulse, respiration and blood pressure changes.
  • When coma and respiratory difficulties occur, timely oxygen can be administered, and tracheal intubation and ventilator-assisted ventilation can be performed.
  • Suspend eating and drinking if vomiting.
  • Keep the skin clean, turn over regularly, and use air cushion or soft cushion on the parts that are easy to be pressurized to prevent pressure sores from occurring.
  • Medication

    Antihypertensive drugs

  • Commonly used intravenous drugs: sodium nitroprusside, nicardipine, mifepristin (Afonate), magnesium sulfate.
  • Commonly used oral drugs: nifedipine, valsartan, amlodipine and so on.
  • Precautions:
  • Antihypertensive treatment should be rapid, so that the blood pressure is maintained at about 160/100mmHg, but the amplitude should be paid attention to, to avoid causing hypoperfusion and cerebral infarction.
  • After intravenous blood pressure reduction reaches the target level, change to oral antihypertensive drug treatment.
  • Dehydration drugs

  • Therapeutic purpose: reduce cerebral edema, relieve headache, vomiting and other symptoms.
  • Commonly used drugs: mannitol, methylprednisolone, dexamethasone, etc.
  • Precautions:
  • Peptic ulcer, elevated blood sugar, dyslipidemia, hyponatremia, and renal impairment may occur.
  • Urine output, blood glucose, blood lipids, electrolytes, etc. need to be monitored during medication.
  • Other drugs

  • Antiepileptic drugs: such as sodium valproate, diazepam, phenobarbital, chloral hydrate. Care should be taken to avoid adverse reactions such as respiratory depression.
  • If headache symptoms are obvious, analgesic drugs such as codeine and aminophenol hydrocodone can be used.
  • Prognosis

    Cure

  • Most patients have a relatively good prognosis after timely and active blood pressure lowering treatment and stable blood pressure control.
  • The prognosis of patients with complications such as acute cerebral hemorrhage, massive cerebral infarction, epileptic status, renal failure, etc. is poorer. Sequelae such as hemiplegia, aphasia, blindness, cardiac and renal injury may remain.
  • Prognostic factors

    The prognosis is relatively good in the presence of the following conditions.

  • Increased blood pressure and relatively mild symptoms at the onset of the disease.
  • A short history of hypertension with good daily control.
  • Fewer underlying medical conditions.
  • Young age.
  • Hazards

  • If symptoms are severe it may result in limb weakness, paralysis, visual impairment, and prolonged bed rest, leading to a severe reduction in quality of life.
  • A long history of hypertension may cause damage to the heart, kidneys, and other organs.
  • Daily

    Daily Management

    Dietary management

  • Balanced nutrition with low salt and low fat diet.
  • Avoid amine-rich foods such as pickles, bacon, sausages, over-smoked foods, fried and battered foods.
  • Take enough fluids and keep your bowels clear.
  • Do not drink alcohol and avoid excessive consumption of strong tea and coffee.
  • Life Management

  • Pay attention to rest, maintain a good daily routine, do not smoke, do not stay up late, do not overwork, etc..
  • Adhere to home rehabilitation training and moderate exercise after discharge from the hospital.
  • Closely monitor and strictly control blood pressure.
  • If you need to use MAOI drugs, postganglionic sympathetic inhibitor drugs, you need to strictly follow the doctor’s instructions.
  • Follow-up and review

  • Follow up and review regularly as prescribed by the doctor. Focus on monitoring blood pressure, headache, limb movement and sensory loss and other symptomatic changes.
  • Follow-up content: Mainly review blood pressure, general condition, neurological signs, cranial MRI and other examinations.
  • Prevention

    The prevention of this disease is based on controlling blood pressure.

  • Control the weight and waist circumference within the normal range.
  • Avoid adverse emotions such as tension and anxiety.
  • Undergo regular physical examination, paying particular attention to blood pressure, ECG, echocardiography and other tests.
  • Actively treat hypertension-related underlying diseases, such as sleep apnea syndrome, hyperlipidemia, renal disease, endocrine disease, cardiovascular disease and so on.
  • Seek prompt medical attention when headache, dizziness, nausea, vomiting and unfavorable limb movement occur.