Cerebral hemorrhage refers to primary non-traumatic intracerebral parenchymal hemorrhage.
1. Etiology, pathogenesis and pathology
1, etiology: the majority of cerebral hemorrhage is caused by hypertension combined with small arteriosclerosis; other etiologies include aneurysm, arteriovenous malformation, cerebral amyloid angiopathy, cerebral arteritis, infarct cerebral hemorrhage, anticoagulation or thrombolytic therapy, Moyamoya disease, entrapment aneurysm, hematologic diseases (leukemia, aplastic anemia, thrombocytopenic purpura, hemophilia, erythrocytosis and sickle cell disease, etc.), and primary or metastatic tumors. ), and primary or metastatic tumors, etc.
2.Pathogenesis: Although hypertension is the most common cause of cerebral hemorrhage, the pathogenesis is not completely clear. At present, it is mostly believed that long-term hypertension can lead to sclerosis of small arteries or deep penetrating branch arteries in the brain, fibrinoid necrosis or lipid hyaline degeneration of the vessel wall, formation of small aneurysms or intercalated aneurysms; when the blood pressure rises suddenly there is rupture and bleeding of the diseased vessels, or blood leaks out from the vessel wall and blood enters the brain tissue to form hematoma. Another possible mechanism is that hypertension can cause spasm of small distal vessels, resulting in, for example, hypoxic necrosis of the vessel wall, which leads to hemorrhage. The wall of the internal cerebral artery has fewer middle layer myocytes and outer membrane connective tissue, and lacks an outer elastic layer. This structural feature of thin wall may be an important reason for the higher incidence of cerebral hemorrhage than other organs. In addition, under the combined influence of the right angle between the proximal end of the ductus arteriosus and the middle cerebral artery and the long-term high-pressure blood flow impact, the deep penetrating artery has more severe and prominent sclerosis and is more prone to cornual aneurysm, which is also the best site for cerebral hemorrhage, and its lateral branches are often called hemorrhagic arteries.
A bleed usually lasts less than 30 min, but data show that about 20% to 40% of cerebral hemorrhages continue to expand within 24 h after the disease, and massive bleeding can directly cause the patient’s death. Multiple cerebral hemorrhages are rare and usually occur secondary to hematologic disease, cerebral amyloid angiopathy, vasculitis, neoplastic or sinus venous occlusive disease.
Hematomas are mostly single foci of hemorrhage, usually around 2 to 8 cm, and multifocal hemorrhage is rare. The brain tissue around the hematoma is obviously compressed and edematous; when the hematoma is large, it causes displacement and deformation of brain tissue and ventricles, such as a large hematoma in the supratentorial hemisphere can squeeze down the hypothalamus and brainstem, causing deformation and displacement and secondary hemorrhage, and in severe cases, herniation of the cerebellar curtain; the downward displacement of midline structures such as the hypothalamus and brainstem can form central herniation; if the intracranial pressure is significantly increased or a large amount of cerebellar hemorrhage can easily occur occipital foramen herniation, which are all causes of cerebral hemorrhage These are the direct causes of brain hemorrhage and death.
In the acute phase, the center of the hemorrhagic foci is filled with blood or purple grape pulp-like clots, surrounded by necrotic brain tissue and stasis-like hemorrhagic softening bands; after the acute phase, the clots dissolve, iron-containing heme and necrotic brain tissue are removed by phagocytes, gliosis proliferates, small hemorrhagic foci form glial scar, and large hemorrhagic foci can form stroke sacs.
2.Clinical manifestations
The general features are most common in hypertensive patients over 50 years of age. It usually occurs during emotional excitement and activity, is slightly more common in men, and has more onset in winter and spring. Most of the patients have no warning before the disease, but a few patients may have headache, dizziness, limb numbness and other prodromal symptoms. The onset of the disease is sudden and often peaks within minutes to hours, manifesting as focal symptoms such as hemiparesis, aphasia and hemianesthesia, often accompanied by intracranial hypertension symptoms such as headache, nausea and vomiting and significant elevation of blood pressure, and severe cases may turn into confusion or coma within minutes.
3.Auxiliary examination
CT examination is the first choice for clinical diagnosis of cerebral hemorrhage, which immediately shows a round or ovoid homogeneous high-density area with clear borders after the onset of ICH; it can also clarify the site, size and shape of the hematoma, whether it has broken into the ventricles or displaced brain tissue, the degree of cerebral edema and obstructive hydrocephalus, which can help confirm the diagnosis and guide the treatment. In case of progressive disease, CT dynamic observation should be performed. A large amount of blood accumulation in the ventricles shows a high-density cast and enlargement of the ventricles. There is circumferential enhancement around the hematoma after one week, and the hematoma appears hypointense or cystic after resorption. In patients with severe anemia, the hemorrhagic focus may show isointense or slightly hypointense changes.
The diagnosis of brainstem hemorrhage is better than CT, but the diagnostic value of supratentorial and cerebellar hemorrhage in the acute stage is not as good as CT; when CT cannot identify cerebral hemorrhage after 4-5 weeks of disease, MRI can still clearly distinguish it, so it can differentiate old cerebral hemorrhage from cerebral infarction. MRI is more likely to detect cerebrovascular malformations, hemangiomas and tumors and other causes of hemorrhage than CT.
If cerebrovascular malformation, Moyamoya disease, or vasculitis is suspected, cerebral angiography should be performed to clarify the diagnosis or interventional treatment.
4.Treatment
In the acute stage, the main goal is to prevent further bleeding, reduce cerebral edema and intracranial hypertension, and prevent and treat complications.
Internal medicine treatment
1.Advocate treatment in the vicinity, avoid moving as much as possible; keep quiet, rest in bed, reduce visits; keep the airway open, clear respiratory secretions in time, inhale oxygen if necessary; if there is high fever, active cooling treatment; strengthen care, keep the functional position of the limbs; place the gastric tube nasal feeding as appropriate to ensure nutrition and maintain water and electrolyte balance.
2.Dehydration to lower cranial pressure and control cerebral edema
3.Control of hypertension
4.Control of complications
Surgical treatment
The following surgical methods are commonly used
①Craniotomy for hematoma removal;
②Borehole enlargement of bone window hematoma removal;
③Tapered hole perforation hematoma aspiration;
④Stereotactic hematoma drainage;
⑤ Ventricular drainage: for ventricular hemorrhage.