parenchymal hemorrhage
Introduction
Introduction Cerebral hemorrhage, also known as cerebral hemorrhage, refers to spontaneous bleeding in non-traumatic brain parenchyma. The causes are various, most of which are caused by rupture of blood vessels caused by hypertension and small arteriosclerosis. Therefore, it is also called hypertensive cerebral hemorrhage. The close relationship between cerebral hemorrhage and hypertension is that about one-third of patients with hypertension have cerebral hemorrhage, and about 95% of patients with cerebral hemorrhage have high blood pressure. Cerebral hemorrhage is a common acute cerebrovascular disease in middle-aged and elderly people, with high mortality and disability rate. It is the highest clinical type of cerebrovascular disease in China. Cerebral hemorrhage accounts for 40% to 50% of all cerebrovascular diseases. 80% of cerebral hemorrhage occurs in the cerebral hemisphere, and 20% occurs in the brain, brainstem, cerebellum, and ventricles.
Cause
Cause
Hypertensive atherosclerosis is the most common cause, generally older, and has a younger trend in recent years. In addition, aneurysms, vascular malformations, infections, etc. can also cause bleeding in the brain parenchyma, and is the main cause of non-traumatic bleeding in adolescents. Tumors can also be combined with bleeding, sometimes masking the tumor itself. Premature infants, hemorrhagic infarction, coagulopathy and iatrogenic anticoagulant therapy can cause hemorrhage of the brain.
Examine
an examination
Related inspection
Brain CT examination brain MRI examination EEG examination brain nerve examination
Often acute onset, with increased intracranial pressure and nerve compression symptoms, a small amount of bleeding can be similar to cerebral infarction without significant increase in intracranial pressure. Because the edema will reach a peak within 2 weeks, the symptoms tend to gradually increase.
Location: Hypertensive hemorrhage is mostly located in the basal ganglia, thalamus, brainstem, etc., and the cerebral cortex and cerebellum are rare.
Hematoma evolution:
(1) Hyperacute period: 4-6 hours, the red blood cells are perfect, containing oxygenated hemoglobin; the blood gradually solidifies and the serum is extruded.
(2) Acute phase: 7h3d, red blood cells are deformed but the cell membrane is intact, Hb evolves into deoxyhemoglobin; edema is aggravated.
(3) Subacute phase: In the early stage (4d~7d), the Hb developed from the periphery to the center evolved into methemoglobin; in the late stage (7d~2w), the red blood cells ruptured and the methemoglobin overflowed. An inflammatory repair reaction occurs around the hematoma in this period.
(4) Chronic phase: After 3w, the hematoma around the hematoma evolved into hemosiderin, and the hematoma began to absorb, and the surrounding glial cells proliferated. After 1 m, the hematoma began to evolve into a softening lesion.
Corresponding imaging performance:
(1) CT: The density of hematoma in the hyperacute and acute phases gradually increased with the formation of blood clots, and edema and occupying place were also aggravated. The density around the subacute hematoma began to decrease, and the hematoma gradually went from high to low to low density. The edema and occupying position also gradually subsided from the peak of 2w. In this period, the periphery could be strengthened by ring and it was a bull's eye sign. Chronic hematoma gradually evolved from low density to softening, with a negative mass effect.
In addition, the bleeding of anemia patients is slightly higher due to the lack of hemoglobin. Patients with coagulation disorders may not coagulate and resemble intravascular blood, and may also have a liquid-liquid level due to sinking of blood cells.
(2) MRI: The edema occupying position is the same as CT. Oxygenated hemoglobin is T1 and other signals T2 high signal; deoxyhemoglobin is T1 and other signals T2 low signal; intracellular methemoglobin is T1 high signal T2 low signal; extracellular methemoglobin is T1 high signal T2 high signal; The flavin is a signal T2 low signal such as T1.
Diagnosis
Differential diagnosis
The following symptoms need to be identified when symptoms of parenchymal hemorrhage occur.
(1) Identification of high density: identification with calcification and high-density tumor or granuloma, calcification CT value is more than 100HU, hematoma is more than 95HU; high-density tumor CT value is more than 60HU, hematoma evolves to below 60HU edema Often more obvious, but not as obvious as metastatic tumors, it is difficult to identify when strengthening or MRI. High-density non-swelling metastases are sometimes difficult to identify with bleeding. Infarction bleeding is sometimes difficult to identify with granulation in the infarct.
(2) Identification of bleeding causes: Hypertensive hemorrhage has a typical medical history and typical bleeding sites. Hemorrhage of the aneurysm combined with subarachnoid hemorrhage mainly at the site of the aneurysm. Arteriovenous malformations can be seen in vessels of equal density and distortion. MayaMaya has multiple bleeding and infarctions at the same time, and most of them are adolescents. The tumor combined with hemorrhage often saw a slightly higher density tumor with equal density or lower than bleeding. It is most important to improve the cause of discriminating and remind patients to undergo MRI. MRI is often diagnosed because of the large difference between the bleeding signal and the cause signal.
