The latest standard for cerebral hemorrhage staging_cerebral hemorrhage staging time

Generally, there will be no bleeding in the brain unless it is caused by some diseases. Cerebral hemorrhage is divided into different time periods, which is generally related to the individual's physical health. It also includes the processes of hemorrhagic necrosis. Clinically, cerebral hemorrhage can be divided into right damage, cerebral edema, cerebral ischemia and various complications.

Cerebral hemorrhage staging time

The ideas of individualized treatment of stroke and classification and staging of treatment of cerebral infarction proposed in recent years have received widespread attention from all parties, but the classification and staging of treatment of cerebral hemorrhage has not received enough attention.

In my country, the proportion of cerebral hemorrhage in stroke is much higher than that in foreign countries, and cerebral hemorrhage is the stroke with the highest mortality rate, so its early treatment is crucial. Since cerebral hemorrhage has significant clinical signs, it can be diagnosed promptly by imaging such as CT, which is conducive to early treatment and timely selection of appropriate treatment plans.

A large amount of clinical practice has proved that the treatment of cerebral hemorrhage, like cerebral infarction, must follow the principle of individualization in order to effectively reduce the mortality and disability rates and improve the overall treatment level.

1 Clinical pathology

The acute expansion caused by cerebral hemorrhage causes ischemia of local microvessels due to mechanical compression, which, together with the damaging effects of blood decomposition products, causes edema, degeneration, and necrosis of brain tissue. Experiments have shown that after 30 minutes of bleeding, the surrounding substance undergoes spongy changes (spongy layer), and after 6 hours the tissue close to the hematoma undergoes necrosis (necrotic layer). Outside the necrotic layer, there are the extravascular hemorrhage layer and the spongy layer. After 12 hours, the necrotic layer and the extravascular hemorrhage layer merged into a sheet.

It can be seen that within 12 hours of bleeding, the surrounding tissues show degeneration, bleeding and necrosis. This pathological process becomes the theoretical basis for early treatment.

The clinical manifestations of cerebral hemorrhage can basically be divided into signs of global brain damage, signs of local lesions and secondary visceral dysfunction, all of which have corresponding pathological bases.

1 Cerebral hematoma Bleeding forms a hematoma in the brain, with a blood clot and necrotic brain tissue in the center, and an ischemic edema area around it, with a penumbra in the middle. These pathological changes become the pathological basis of focal brain damage and clinical guidelines.

2 Cerebral ischemia and hematoma compress the surrounding brain tissue, causing severe ischemia, increased vascular permeability, damage to vessel walls, and seepage or leakage of blood components, which become important reasons for the continuous expansion of the central necrotic area. In some cases, the ischemic volume may be several times larger than the hematoma, further aggravating cerebral edema, leading to intracranial hypertension, and inducing insufficient blood supply to other brain regions far away from the hematoma, or even the entire brain.

3 Brain edema starts as local edema, which quickly spreads to the entire brain, mainly in the white matter. In the early stage, it is basically vasogenic edema due to damaged blood-brain barrier, while in the later stage, it is combined with cytotoxic edema. If the hematoma is close to or breaks into the ventricle, it can easily cause cerebrospinal fluid circulation disorders, which can aggravate intracranial hypertension and cerebral edema. The latter two in turn aggravate global cerebral ischemia, forming a vicious circle.

4 Secondary damage, hematoma, cerebral edema and intracranial hypertension can cause compression and displacement of adjacent brain tissue, resulting in brain herniation. It can also damage the hypothalamus, leading to central hyperthermia, upper gastrointestinal bleeding, metabolic and electrolyte disorders, etc. Combined with factors such as drugs (such as dehydrating agents), changes in immune function, and concurrent infections, it can cause dysfunction of the heart, kidneys, lungs, and even multiple organ failure.

To sum up, the clinical signs of patients with cerebral hemorrhage are mainly determined by the location and size of the hematoma, and the severity of secondary ischemia, edema, cerebrospinal fluid circulation disorders, intracranial hypertension, etc. The severity of the original hypertensive cerebral arteriosclerosis and the corresponding compensatory capacity of the collateral circulation may also affect the clinical manifestations.

It can be seen that the intracranial lesions vary from patient to patient. In addition, the overall state, especially changes in visceral function, also varies greatly and can vary greatly in different stages of cerebral hemorrhage. These have become the basic basis for the individualized treatment principle.