Hypertensive encephalopathy
Introduction
Introduction to Hypertensive Encephalopathy The disease is seen in patients with hypertension, an acute cerebrovascular disease that causes severe cerebral edema due to sudden and sudden increase in arteries, leading to loss of control of cerebral arteriolar spasm or cerebrovascular regulation. Any type of high blood pressure can cause hypertensive encephalopathy as long as the blood pressure is significantly increased, but it is more common in patients with normal blood pressure and sudden high blood pressure, such as acute glomerulonephritis, pregnancy poisoning, etc. Or patients with severely progressive hypertension with significant cerebral arteriosclerosis. In addition to sudden increase in blood pressure, often accompanied by severe headache and mental changes, sometimes physical activity disorders, fundus examination has limited or diffuse retinal arteriospasm, but not necessarily bleeding, exudation or edema, after antihypertensive treatment Can be quickly restored. basic knowledge The proportion of illness: 0.02%-0.05% Susceptible people: more common in the elderly Mode of infection: non-infectious Complications: cerebral palsy cerebral thrombosis cerebral hemorrhage
Cause
Causes of hypertensive encephalopathy
Essential hypertension (25%):
The incidence of essential hypertension accounts for about 1%, the history of hypertension is longer, and those with obvious cerebral arteriosclerosis are more likely to occur. The blood vessels with normal blood pressure and sudden high blood pressure, such as acute hypertensive and acute glomeruli Nephritis patients can also occur.
Secondary hypertension (20%):
Such as pregnancy-induced hypertension syndrome, glomerular nephritis hypertension, renal artery stenosis, pheochromocytoma and other high blood pressure, there may be hypertensive encephalopathy.
Some drugs or foods induce hypertensive encephalopathy (20%):
In rare cases, patients with hypertension who use monoamine oxidase inhibitors, while taking Rauvolfia, methyldopa or post-ganglionic sympathetic inhibitors, can also cause symptoms similar to those of hypertensive encephalopathy, eating amine-rich Food can also induce hypertensive encephalopathy.
After carotid endarterectomy (20%):
After carotid endarterectomy in patients with high carotid stenosis, sudden increase in cerebral perfusion can also cause hypertensive encephalopathy.
(two) pathogenesis
The pathogenesis of hypertensive encephalopathy has not yet been fully elucidated. There are two theories:
1. Over-regulation or arteriolar spasm: Under normal circumstances, cerebral blood vessels shrink and contract with blood pressure. When blood pressure rises, blood vessels in the brain contract; when blood pressure drops, cerebral blood vessels dilate, when the blood pressure rises sharply, it can cause meninges and Perpetual paralysis of the small arterioles of the brain reduces the blood flow into the capillaries, leading to increased ischemia and capillary permeability, increased extravasation of blood in the blood, which can lead to cerebral edema and increased intracranial pressure, which can occur on this basis. Necrotizing arteriitis, punctate hemorrhage or multiple small embolism, causing acute cerebral blood circulation disorder and brain function damage, resulting in a series of clinical manifestations.
2, automatic regulation of rupture theory: cerebral blood vessels usually expand or contract with changes in blood pressure, in order to maintain the relative stability of cerebral blood flow, direct measurement of the diameter of meningeal blood vessels and indirect measurement of cerebral blood flow with isotopes, indicating meningeal blood vessels when blood pressure drops Expansion, when the blood pressure rises, it shrinks. In normal people, when the mean arterial pressure (MAP) is between 60 and 120 mmHg, the cerebral blood flow is constant, and the blood pressure is obviously increased. For example, when MAP 180 mmHg, the automatic regulation mechanism is destroyed, and the original contraction is performed. The cerebral blood vessels (contraction when blood pressure rises) suddenly expand due to the inability to withstand excessive pressure, resulting in so-called passive expansion. As a result, cerebral blood vessels are over-perfused, cerebral blood flow is increased, plasma osmotic pressure is increased, and blood is permeated around the blood vessels. Edema and intracranial hypertension produce a range of clinical manifestations.
The main pathological change of this disease is diffuse cerebral edema. The increase of brain weight can exceed 20%~30% of normal brain. The brain looks pale, the brain is flattened, the sulcal area becomes shallow, the ventricle becomes smaller, and the superficial part of the brain is arteries. Vascular and venous dilatation, Virchow-Robin cavity enlargement, white cut surface, may have sputum hemorrhage or small narrow fissure hemorrhage and lacunar lesions, etc., glassy degeneration of cerebral arterioles wall thickens vascular endothelium Adventitial hyperplasia, vascular stenosis or obstruction, resulting in fibrinous thrombosis and microinfarction of the brain parenchyma, forming a unique arteriolopathy of the disease, fibrinous cell necrosis of the vessel wall can be severely ruptured, and most defects or brains occur. Internal hemorrhage, Feigin and Prose (1959) describe two types of cerebral arterial degeneration, one is fibrin-like arteritis, visible vascular wall inflammatory changes, blood extravasation, microaneurysm formation; another kind of blood vessel wall is not inflammatory Sexual changes, collagen staining substances narrow the vascular lumen, small thrombosis and cerebral ischemia, increased intracranial pressure or increased retinal arterial pressure impede venous return, can lead to retinal artery cellulose Death, infarction or hemorrhage and permanent loss of vision, but also visible swelling oligodendrocytes, dendritic cell disruption (clasmato-dendrosis) and ischemic changes in neural element.
Prevention
Hypertensive encephalopathy prevention
Hypertensive encephalopathy is a very dangerous disease, with brain damage being the most prominent. It must be rescued in time. Anyone with high blood pressure who has a sharp rise in blood pressure with severe headache, or even conscious and altered minds should immediately go to the hospital for emergency treatment. To quickly control blood pressure in a safe range, to prevent or reduce brain tissue edema and injury is the key to treatment. In addition, in the course of treatment, excessive blood pressure should be avoided to cause blood perfusion in the brain, heart and kidney, and systemic treatment of hypertension and The primary disease, avoiding overwork and mental stimulation will help reduce the incidence of hypertensive encephalopathy. After the disease is stable, it should gradually transition to conventional antihypertensive treatment and adhere to long-term, regular treatment.
Complication
Hypertensive encephalopathy complications Complications cerebral cerebral thrombosis cerebral hemorrhage
Easy to have cerebral palsy, rare with cerebral thrombosis or cerebral hemorrhage.
1, cerebral palsy: due to increased brain edema, its brain volume increased and oppressed normal brain tissue, prone to cerebral palsy, can quickly die.
2, cerebral thrombosis or cerebral hemorrhage: Schwartz et al reported that among 110 cases of hypertensive encephalopathy, 3 cases of fatal cerebral hemorrhage caused by thrombocytopenia, although the complications of cerebral hemorrhage are rare, but the consequences are serious.
Symptom
Symptoms of hypertensive encephalopathy Common symptoms Hypertension coma, dyspnea, over-stress, increased intracranial pressure, cervical rigidity, dysfunction, loss of consciousness, loss of dehydration
Sudden onset, the disease is developing very rapidly. People with impaired renal function are more likely to develop the disease.
First, the arterial pressure increased: the original high blood pressure, before the onset, increased again, diastolic blood pressure of more than 16Kpa, the average arterial pressure is often between 20.0 ~ 26.7kpa.
Second, increased intracranial pressure: caused by brain edema. The patient had severe headache, jet vomiting, papilledema, retinal arterial spasm with flame-like hemorrhage and arterial spasm and villous exudate.
Third, the disturbance of consciousness: can be expressed as lethargy and coma, mental disorder has also occurred.
Fourth, seizures: may be systemic localized seizures, and some have epileptic continuous state.
Fifth, paroxysmal dyspnea: caused by respiratory central vasospasm, ischemia and acidosis.
Sixth, other symptoms of brain dysfunction: such as aphasia, hemiplegia and so on.
Laboratory tests show increased cerebrospinal fluid pressure (prohibited when the diagnosis is clear), and cellular and protein levels can also be increased.
Examine
Examination of hypertensive encephalopathy
Laboratory inspection
1, unless accompanied by kidney disease or uremia, urine routine usually no protein, red blood cells, white blood cells and casts, blood urea nitrogen is normal.
2, CSF pressure increased most, even normal, the number of cells is normal, very few patients have a small amount of red blood cells, protein slightly increased.
Film degree exam
Imaging studies of the skull are important for diagnosis.
1. Brain CT: There is limited or extensive low-density focal cerebral edema, mainly involving subcortical white matter, and occasionally involving the cortex. Schwartz et al found that hypertensive encephalopathy complicated by hypertension, cerebral edema is often bilateral, mainly Located in the occipital lobe, there are also the stellate structures in the parietal lobe, the posterior frontal lobe, and the cerebellar corpus callosum. The hypertensive encephalopathy after carotid endarterectomy, the cerebral edema is located in the anterior cerebral artery, the middle artery blood supply area, and the high After the remission of blood pressure encephalopathy, CT abnormalities disappeared.
2. Brain MRI: Similar to CT changes, T1 decreased and T2 increased on MRI.
3, SPECT: In the CT or MRI showed abnormal parts, blood perfusion increased.
4, fundus examination: retinal artery is diffuse or localized, strong sputum, hardening or bleeding, exudation and optic disc edema.
5, EEG: there are localized abnormalities or bilateral synchronous sharp slow waves, sometimes showing poor rhythm.
Diagnosis
Diagnosis and diagnosis of hypertensive encephalopathy
According to the sudden increase of blood pressure and symptoms of intracranial pressure in patients with hypertension, the diagnosis is not difficult and needs to be differentiated from other acute cerebrovascular diseases.
(1) The blood transfusion of the lumbar cerebrospinal fluid can confirm the diagnosis.
(2) subarachnoid hemorrhage: like hypertensive encephalopathy, there may be sudden severe headache, vomiting, meningeal irritation, some patients may also have increased blood pressure, conscious disturbance is usually light, rarely hemiplegia, and cerebrospinal fluid is even Blood and other characteristics can be identified with hypertension.
(3) intracranial space-occupying lesions: although there are severe headaches, but slowly, non-sudden occurrence, other symptoms of increased intracranial pressure and focal neurological signs are progressive elevation of blood pressure, although elevated, but not high Significantly increased blood pressure encephalopathy.
(4) If the clinical suspected intracranial tumor can be diagnosed by brain ultrasound, cerebral angiography or CT examination.
