I. Overview of cerebrovascular disease
Cerebrovascular disease refers to a group of diseases in which intracranial ischemia or hemorrhage occurs on the basis of lesions or hemodynamic disorders in the vessel walls supplying the brain and causes transient or persistent local or diffuse brain damage, resulting in a series of clinical manifestations. Cerebrovascular disease is divided into acute cerebrovascular disease and chronic cerebrovascular disease according to the urgency of onset, and the former is divided into transient ischemic attack (TIA) and stroke (Stroke), also known as stroke (Apoplexy), cerebrovascular accident, generally including cerebral hemorrhage, cerebral infarction and subarachnoid hemorrhage; according to the nature of the lesion can be divided into hemorrhagic cerebrovascular disease and ischemic Cerebrovascular disease, the former including cerebral hemorrhage, subarachnoid hemorrhage, the latter including TIA and cerebral infarction.
II. Hemorrhagic cerebrovascular disease (cerebral hemorrhage)
Cerebral hemorrhage (CH), also known as cerebral hemorrhage, is an acute, spontaneous, non-traumatic hemorrhage that occurs from the blood vessels in the brain parenchyma under the influence of a combination of factors based on the underlying disease. In China, cerebral hemorrhage accounts for 20-40% of all cerebrovascular diseases, and is a clinical type with high morbidity, disability and mortality.CH is divided into primary and secondary CH.
[Etiology and pathogenesis
1, etiology The main causes of cerebral hemorrhage are hypertension and cerebral atherosclerosis, followed by amyloid cerebrovascular disease, hypertension is the most important independent predictor of CH, about 60% ~ 70% of primary CH patients have hypertension. Amyloid cerebrovascular disease (CAA) often causes lobar hemorrhage and is prone to recurrence. Other etiologies include: cerebrovascular malformations, aneurysms, arterial entrapment, Moyamoya disease, cerebral arteritis, cerebral venous system thrombosis, hematologic disease, and medical origin. Less common are intracranial tumors, drugs, drug abuse, etc. Some causes of cerebral hemorrhage are unknown.
2.Pathogenesis Cerebral blood vessels have their own characteristics, the wall is relatively weak, the outer membrane of the middle membrane is not developed, lack of elastic layer, hypertension, atherosclerosis can cause changes in the structure of the wall, the formation of tiny aneurysms or arterial lipid hyaline degeneration, deep penetrating arteries are more likely to be involved, when the blood pressure fluctuation is large, easy to rupture and bleeding, so it is the main site of bleeding. Regardless of the cause of bleeding, there is an underlying lesion of the vessel itself in the first place. Under the influence of a combination of factors based on the underlying disease, the lesioned vessel ruptures and bleeds and forms a hematoma, which early on mechanically compresses the surrounding brain tissue, causing brain tissue displacement, high cranial pressure, edema, and ischemia and hypoxia, which easily forms a vicious circle and finally leads to brain herniation formation. The pathophysiological understanding of CH has changed somewhat in recent years. In the past, cerebral hemorrhage was considered to be a simple, rapid, one-way process, and the hemorrhage was thought to stop within minutes of the start. The current view is that it is a dynamic, complex process involving different phases, i.e., early hematoma expansion: the hemorrhage is continuous, and the hematoma continues to expand within a few hours after the onset of symptoms, occurring mainly within 6 h. After 6 h, the hematoma tends to stabilize. the mechanisms leading to early hematoma expansion in the acute phase of CH are not well understood, and most people believe that they are related to hypertension, high cranial pressure, local brain tissue compression Most people believe that it is related to hypertension, high cranial pressure, local brain tissue compression, multifocal hemorrhage, and our clinical finding that patients with long-term alcoholism, abnormal liver function, and abnormal blood clotting mechanisms are more likely to have hematoma enlargement than patients without these factors. Brain damage around the hematoma generally occurs within a few days after CH, and secondary damage to brain tissue caused by hematoma breakdown products during the hematoma resorption period is thought to be related to thrombin and other coagulation-related end products-mediated brain damage and brain edema. The condition peaks 24-48 hours after cerebral hemorrhage, then stabilizes and gradually recovers slowly. Since the symptoms of neurological deficit are mainly caused by hematoma and edema compression, there will be considerable recovery of neurological function.
Clinical manifestations
Patients mostly have acute onset under activity and emotional agitation, or without obvious triggers. Generally, they have obvious whole-brain symptoms, such as headache, vomiting, impaired consciousness, as well as neurological dysfunction such as hemiparesis, hemiplegia, hemianopsia, aphasia, seizures, etc., which are progressively aggravated and blood pressure is elevated at the onset. Clinical manifestations depend on the amount of bleeding and the site of bleeding, of which changes in consciousness are the main basis for judging the severity of the disease. There are mostly localized signs of the nervous system, and some patients may have signs of meningeal irritation.
Clinical types and characteristics of cerebral hemorrhage
Hemorrhage in the basal ganglia region is the most common site of hypertensive cerebral hemorrhage and is mostly caused by rupture of the lateral pudendal artery. Compression of the internal capsule by the hematoma may cause the typical triple deviation sign, gaze to the side of the lesion in both eyes, and aphasia in the dominant hemisphere. Thalamic hemorrhage is caused by rupture of the thalamic geniculate artery or the thalamic penetrating artery. The typical symptoms are hemianesthesia, mild paralysis, and aphasia or aphasia syndrome; the hemorrhage is large, and when it breaks into the ventricle, there is a heavy impairment of consciousness, both eyes often gaze inward or downward, and the pupils are unequal in size bilaterally, usually scattered on the hemorrhagic side, indicating the formation of herniation of the cerebellar curtain. The brain is tonic, with central hyperthermia and vomiting of coffee-like gastric contents. Hemorrhage in the head of the caudate nucleus is usually caused by rupture of the Heubner’s regurgitant artery and has mild clinical symptoms.
Lobar hemorrhage accounts for about 10% of cerebral hemorrhage, mostly caused by vascular malformations such as arteriovenous malformations, moyamoya disease, and tumors in young people, and commonly caused by hypertensive arteriosclerosis in the elderly, followed by amyloid-like vascular disease. Clinical symptoms can be divided into three groups: those without paralysis and somatosensory disorders: headache, vomiting, meningeal irritation and bloody cerebrospinal fluid need to be distinguished from subarachnoid hemorrhage; those with paralysis and/or somatosensory disorders; and those in coma at the onset. The frontal lobe has psychotic symptoms, strong grip and groping; the temporal lobe has hallucinations, sensory aphasia, etc.; the parietal lobe has sensorimotor disorders (mostly single limb), loss of use, body orientation disorders; the occipital lobe has cortical blindness, etc. The hemorrhage should be differentiated when it easily breaks into the subarachnoid space.
Pontine hemorrhage accounts for about 10% of cerebral hemorrhage. Small amount of hemorrhage (light): clear consciousness, facial and spreading nerve cross paresis, bilateral eye gaze to the opposite side of the lesion; large amount of hemorrhage (>5m1, heavy): early and heavy coma, flaccid paresis of limbs, bilateral pupils are pinpoint, central hyperthermia, irregular breathing, and death within 24~48 hours.
Cerebellar hemorrhage accounts for about 10% of cerebral hemorrhage, with sudden onset; marked vertigo, frequent vomiting; occipital pain; ataxia on the lesion side; nystagmus; ipsilateral peripheral facial palsy; cervical tonicity; marked increase in intracranial pressure, deepening coma, and death by occipital foramen herniation. Small amount of hemorrhage has mild symptoms and quick recovery.
Primary ventricular hemorrhage (cerebral ventricle hemorrhage): primary refers to the choroid plexus vascular hemorrhage and subventricular canal hemorrhage within 1.5 cm into the ventricle, previously thought to be rare, now confirmed to account for 3% to 5% of cerebral hemorrhage. Mild type: headache, vomiting, strong collar, Kernig’s sign (+), resembling subarachnoid hemorrhage; heavy type: all the ventricles are filled with blood, the onset of deep coma, vomiting, extremely narrow pupils, two eyes separated strabismus or floating eyes, flaccid paralysis of the limbs, may have decerebral tonicity, deep breathing, snoring, significantly elevated body temperature, facial congestion and sweating, serious prognosis, more rapid death.
Primary ventricular hemorrhage accounts for 3-5% of cerebral hemorrhage and is caused by rupture of the choroid plexus artery or subventricular artery, or secondary hemorrhage. The symptoms vary greatly among individuals, and most of those with poor cerebrospinal fluid circulation in ventricular casts have a poor prognosis, while those with small amounts of bleeding have a better prognosis.
Related tests
1.CT of the head: the first choice for cerebral hemorrhage, can immediately show high-density shadow and determine the location of the hemorrhage, the size of the hematoma, cerebral edema and ventricular system, which is important for guiding the treatment to determine the prognosis. The disadvantage is that it does not show the subcurtain structures well, and it is easy to miss the bleeding lesions in the cerebellum and brainstem.
2.Head MRI: The MRI performance of cerebral hemorrhage is different in different periods, which can determine the time of hemorrhage; can find small amount of hemorrhage in brainstem or cerebellum that cannot be determined; can distinguish old cerebral hemorrhage and cerebral infarction; shows the flow-space effect of abnormal blood vessels, and can do MRA, MRV, etc. to determine the presence of abnormal blood vessels cerebral angiography (DSA): to find the cause of hemorrhage.
3.Transcranial ultrasound Doppler (TCD) examination: to understand the condition of intracranial arterial blood flow, can obtain information on cerebral vasospasm; can determine intracranial hypertension and brain death; can show intracranial blood flow asymmetry when the blood is larger, i.e., intracranial pressure asymmetry.
4.Lumbar puncture: performed with caution, the cerebrospinal fluid pressure is increased and is mostly bloody; it is no longer used as a routine examination.
5.Digital subtraction cerebral angiography (DSA): it can detect spontaneous hemorrhage caused by aneurysm, arteriovenous malformation, Moyamoya disease, etc.
6.Electroencephalogram: Hemispheric hemorrhage can be widely abnormal, with significant disease side, mostly slow wave.
7. Routine examination: blood and urine routine, blood sugar, renal function, etc.
Diagnosis and differential diagnosis
1.Diagnosis Sudden onset of hypertension in middle-aged and elderly patients during activity or excitement, with varying degrees of headache, vomiting, impaired consciousness and other symptoms, accompanied by focal localization signs such as hemiparesis, hemianesthesia, aphasia, etc. The clinical diagnosis can be made with rapid development of the disease, and cranial CT is required to confirm the diagnosis.
2. Differential diagnosis In the absence of cranial CT, it is necessary to differentiate from the following diseases.
(1) cerebral infarction: cerebral infarction is sometimes not easily distinguished clinically from a small brain hemorrhage cluster, CT examination can confirm the diagnosis, and the distinction is as follows.
Cerebral infarction
cerebral hemorrhage
Age of onset
Mostly above 60 years of age
Mostly under 60 years of age
State of onset
Quiet or during sleep
During activity or excitement
Speed of onset
Peak symptoms within 10 hours or 1-2 days
Peak symptoms within minutes to hours
History of hypertension
Mostly absent
Mostly
Whole brain symptoms
Mild or absent
High cranial pressure symptoms such as headache, vomiting, drowsiness
Disorders of consciousness
Usually mild or absent
More severe
Neurological signs
Mostly non-homogeneous hemiparesis (trunk or branches)
Mostly homogeneous hemiparesis (basal ganglia region)
CT examination
Low-density foci in the brain parenchyma
High-density foci in the brain parenchyma
Cerebrospinal fluid
Colorless and transparent
Hemorrhagic
(2) Traumatic cerebral hemorrhage or subdural artery There is a clear history of trauma and the site of hemorrhage is related to the landing site of the head, usually under the impacted skull or at the site of hedging. Frontal and temporal poles are common, and CT may show hematoma.
(3) Hemorrhage caused by cerebral arteriovenous malformation, aneurysm, Moyamoya disease, intracranial tumor, etc. can have symptoms caused by the original disease, and the condition is suddenly aggravated; CT, MRI, MRA or DSA can identify them.
(4) Hematological disease and medically induced cerebral hemorrhage There is a history of corresponding disease or treatment, and hematological system related examination can assist in the diagnosis.
(5) Coma caused by medical diseases such as diabetes mellitus, hypoglycemia, hepatic coma, uremia, intoxication, drug poisoning, carbon monoxide poisoning, etc. have corresponding medical history and abnormal manifestations of relevant examinations.
Treatment】
1.Treatment principles: prevent hematoma expansion, reduce intracranial pressure, control cerebral edema, maintain vital signs, prevent complications; surgical treatment if suitable for surgery, medical treatment if not suitable for surgery recovery period; promote neurological function recovery.
2.Internal medicine treatment
(1) General supportive treatment and symptomatic treatment: in principle, local consultation and treatment, and try to keep patients quiet and bed rest, especially hypertensive patients. Serious patients should be admitted to NICU, monitor vital signs and closely observe pupil changes. Pay attention to keeping the airway unobstructed, intermittent oxygenation, timely cleaning of respiratory secretions, and timely tracheotomy in case of obstruction to avoid aggravating cerebral edema by hypoxia. Maintain nutrition and water-electrolyte balance, generally require nasal feeding diet after 3 days. Cool down the temperature appropriately, and sub-cold temperature therapy is feasible if available. Strengthen nursing care, keep the affected limb in a functional position, turn regularly, massage regularly, prevent decubitus ulcers and venous thrombosis of the lower limbs, keep the mouth clean and bowels unobstructed.
(2) Blood pressure management: effective control of blood pressure in the acute phase of cerebral hemorrhage can improve the patient’s prognosis, but first deal with high cranial pressure, caused by high cranial pressure is ineffective to lower blood pressure alone. If high cranial pressure is controlled blood pressure is still high can be treated with antihypertensive therapy. Patients with a history of hypertension should maintain a mean arterial pressure of about 130 mmHg; if the blood pressure is measured at an interval of 5 min and the systolic pressure is >230 mm Hg or the diastolic pressure is >140 mmHg on both occasions, sodium nitroprusside is available, if the blood pressure is measured at an interval of 20 min and the systolic pressure is 180-230 mmHg and the diastolic pressure is 105-140 mmHg on both occasions or the mean arterial pressure is ≥130 mmHg, can be intravenous labetalol, esmolol, etc.; such as systolic blood pressure.