1.Spontaneous cerebral hemorrhage is divided into primary and secondary types, what are the characteristics of each of them?
Primary cerebral hemorrhage refers to hypertensive cerebral hemorrhage. Under the effect of long-term hypertension, the blood vessels in the patient’s brain undergo atherosclerosis, glassy degeneration and fibrinoid necrosis of the fine cerebral arteries, or even the formation of microaneurysm or entrapment aneurysm. A sudden rise in blood pressure under the action of certain factors, such as seasonal changes, abnormalities in temperature or climate, and abnormal emotions, can easily lead to blood vessel rupture and bleeding.
The most common causes of secondary cerebral hemorrhage are vascular malformations, such as arteriovenous fistula, cavernous hemangioma, smoldering disease due to chronic occlusion of blood vessels, bleeding from venous sinus thrombosis, bleeding from glioma, papilloma of the choroid plexus in the ventricles, and malformation. In addition, disorders of the coagulation mechanism caused by leukemia, aplastic anemia, hemophilia, thrombocytopenic purpura, and liver disease are also causes of secondary cerebral hemorrhage. As well as cysticercosis of the choroid plexus, this parasitic disease can also cause secondary cerebral hemorrhage.
2. Is intraventricular hemorrhage of primary or secondary type?
There are two types of ventricular hemorrhage. One type is lesions in the ventricles themselves, such as papillomas in the ventricles, hemangiomas in the choroid plexus, and vascular malformations in the choroid plexus, which can cause primary ventricular hemorrhage. The other type is secondary ventricular hemorrhage caused by hemorrhage from other parts around the ventricle, that is, the brain parenchyma, breaking into the ventricle.
3. Is hypertensive cerebral hemorrhage the one with the highest incidence?
Hypertension is the most common cause of cerebral hemorrhage. Long-term underlying hypertensive lesions can cause localized lesions in blood vessels. Hypertensive cerebral hemorrhage is the most common type of cerebral hemorrhage. Cerebral hemorrhage accounts for 20% of all strokes. Strokes include hemorrhagic strokes and ischemic strokes. Ischemic stroke is cerebral infarction and includes cerebral thrombosis, cerebral embolism, and lacunar infarction. Hemorrhagic strokes are divided into subarachnoid hemorrhage and parenchymal hemorrhage, which is cerebral hemorrhage. Cerebral hemorrhage is the most aggressive type.
4. The type of cerebral hemorrhage determines the clinical symptoms of the patient and also predicts the prognosis of the disease, which has a more important significance for the treatment and rehabilitation of the patient. There are many clinical classification methods, and when diagnosing the disease, we need to consider various classification methods to clarify the nature of the disease. What are the types of cerebral hemorrhage that are classified according to the site of hemorrhage?
According to the site of hemorrhage, which is also classified according to the anatomical structure, it can be roughly divided into above the cerebellar curtain and below the cerebellar curtain. Below the cerebellar curtain refers to bleeding in the cerebellum and brainstem. It can be further subdivided into lobar hemorrhage, external capsule hemorrhage, basal nucleus hemorrhage, thalamic hemorrhage, cisternal hemorrhage, caudate nucleus head hemorrhage, ventricular hemorrhage, midbrain hemorrhage, pontocerebellar hemorrhage, medulla hemorrhage, cerebellar hemisphere hemorrhage, cerebellar earthworm hemorrhage, etc.
5.The nucleus accumbens in the basal ganglia is the more common site of hemorrhage, what usually causes it? What are the clinical manifestations of a hematoma in this area?
The most common type of cerebral hemorrhage is basal ganglia hemorrhage. Basal ganglia hemorrhage is divided into nucleus accumbens hemorrhage, thalamic hemorrhage, external capsule hemorrhage, and caudate nucleus head hemorrhage.
Of these, the nucleus accumbens hemorrhage is the most common type, accounting for 60% of cerebral hemorrhage cases. The nucleus accumbens hemorrhage is also called nucleus accumbens hemorrhage because it originates from the middle cerebral artery, which supplies the nucleus accumbens. Patients with shell nucleus hemorrhage often present with contralateral hemiparesis, hemianesthesia, and isotropic hemianopia. Patients also present with bilateral impairment of ipsilateral gaze toward the lesion and gaze to the contralateral side. With hemorrhage in the dominant hemisphere, the patient may also experience aphasia. The most typical symptoms are the “triple hemiplegia” syndrome: hemiparesis, hemianesthesia, and hemianopsia.
Thalamic hemorrhage accounts for 10-15% of these cerebral hemorrhages and is caused by rupture of the thalamic geniculate and thalamic penetrating arteries. It can be a small amount of hemorrhage confined to the thalamus in a few milliliters or a large and aggressive hemorrhage. A large amount of hemorrhage can rapidly break into the ventricles, most likely into the lateral ventricular system. A small amount of blood that breaks into the lateral ventricles can cause a pooling of blood in the lateral ventricles and a large amount of blood can cause a ventricular hemorrhage. Patients with thalamic hemorrhage often present with abnormal sensation in the lateral body, contralateral hemiparesis, and large amounts of hemorrhage can cause hemianopia. Patients may also have specific ocular manifestations, where the patient’s eyes do not look upward, but rather gaze downward, or where the convergence of the eyes is abnormal, or the pupils are narrowed.
Caudate head hemorrhage is usually caused by rupture of atherosclerosis and vascular malformations in hypertension, and the amount of bleeding is usually small and can easily break into the ventricles through the anterior horn of the lateral ventricles. Patients with caudate nucleus head hemorrhage often present with headache, vomiting, cervical tonicity, and psychiatric symptoms, with clinical manifestations much like subarachnoid hemorrhage.
6. For the sudden and high-risk nature of cerebral hemorrhage, a rapid and accurate diagnosis is often required. How do ancillary tests help doctors diagnose the condition?
When faced with a patient with a sudden headache or sudden hemiparesis, the physician first performs a physical examination of the patient. The physician will use the most basic physical examination to determine whether the patient has any impairment of consciousness, hemiparesis, nausea, vomiting, or signs of meningeal irritation. If a brain hemorrhage is suspected, the patient should immediately undergo a CT head examination. CT of the head is the most sensitive, quickest, and most convenient adjunct to the diagnosis of cerebral hemorrhage. According to CT, the amount of hematoma and the location of the hematoma can be determined, and hematoma with a diameter of 0.5 cm or more can be diagnosed quickly.
Nowadays, the resolution of CT is very high, and enhanced CT can quickly detect hematomas of 0.2 cm in diameter. Of course, there is now a special type of brain hemorrhage, namely microhemorrhage. General CT is not easy to detect microscopic amount of hemorrhage, and special examination of MRI is needed. T2* sequence of T2 echo series, or magnetic sensitivity weighted imaging (SWI) sequence is very sensitive to the diagnosis of microhemorrhage.
Microhemorrhages are often caused by many etiologies, and if a patient is found to have microhemorrhages, attention needs to be paid to the use of medications. If medications are not used properly in patients with microhemorrhage, they can induce massive bleeding and make the condition rapidly worse. Other tests, such as MRA and CTA, are used to screen for the presence of vascular malformations, moyamoya disease, narrowing of the middle cerebral artery or abnormal vascular network, and CTA is easier to diagnose structural abnormalities of blood vessels.
7. There are many different forms of cerebral hemorrhage, the site of hematoma and the amount of bleeding are very variable, and in some cases it is necessary to choose surgical treatment. What kind of cases can choose minimally invasive removal surgery for intracranial hematoma?
In the case of a small amount of cerebral hemorrhage, recovery is usually possible with traditional medical medication. The sequelae of brain hemorrhage are related to the site of hemorrhage, for example, 10 ml to 20 ml of external capsule hemorrhage or lobar hemorrhage can have no significant sequelae. The prognosis can vary greatly between 3 ml and 5 ml of medulla oblongata hemorrhage, for example, 15 ml of cerebellar earth hemorrhage or cerebellar hemispheric hemorrhage, the sequelae may be more serious and surgical treatment should be pursued. (The surgical treatment of cerebral hemorrhage has been controversial for many years. A large number of clinical trials and clinical observations have been conducted by medical and surgical departments on the effectiveness of traditional drug therapy and traditional craniotomy for cerebral hemorrhage. There have been some conclusions that craniotomy did not play a significant effect or even was not superior to traditional drug treatment. (Because traditional craniotomy is a major surgery with high trauma and secondary damage from surgery, it is increasingly unacceptable to physicians, so minimally invasive surgery has been gradually developed.)
Minimally invasive hematoma removal is divided into several types: traditional small bone window craniotomy hematoma removal, which is performed by making a small hole in the skull and extracting the blood with a probe that punctures inside the hematoma, and is not less invasive. Because this minimally invasive method cannot aspirate the hematoma cleanly, a new minimally invasive debulking procedure was developed in the 1990s, in which a spiral guidewire is used to mash the hematoma and then the hematoma is drawn out by negative pressure. Although this method attracted the hematoma out, the guidewire could also break the brain tissue and cause more secondary damage. Therefore, this method was also abolished. Gradually, a hard channel YL-1 puncture needle was developed. This is an integrated puncture needle and drainage tube, which is punctured into the hematoma and the core is withdrawn, while the drainage tube remains inside the hematoma.
By using urokinase or other drugs, the hematoma can be liquefied so that it can be gradually aspirated. Compared to soft channel drains, these metal hard channel drains are less likely to be crushed, allowing for gradual drainage of the blood. In addition, the use of a hard channel keeps the skull airtight and rarely causes secondary intracranial infections. There are many advantages of this method: first, secondary trauma is minimal. It does not require craniotomy and stitches, and the puncture needle is only 4 mm in diameter. Second, local anesthesia is used. It does not require general anesthesia, and puncture can be performed even at the NICU bedside. Third, the operation time is very short. It usually takes 20 minutes, and can be finished in half an hour at the longest. Fourth, the cost is very low. It uses a puncture needle of more than one thousand yuan, plus other costs, the total cost of the operation is very low. Fifth, the postoperative recovery is fast. In some patients, the hematoma is cleared by about 70-80% in 3 or 4 days after puncture, and the puncture needle can be removed. Because of these advantages, this procedure is now widely carried out in the emergency departments and inpatient departments of provincial hospitals, prefectural and municipal hospitals, and county hospitals in China. Medical, surgical, and emergency physicians can all perform this procedure.
The core of minimally invasive surgery is to first select different surgical approaches and puncture points according to different bleeding sites. It is important to note that sites such as those where access to the needle is inconvenient, or where access to the needle may cause secondary vascular injury or secondary bleeding are not suitable for the procedure. Second, about the volume of hematoma. In principle, minimally invasive surgery is not advocated for bleeding of less than 30 ml on the curtain, and minimally invasive approach is generally advocated for bleeding of 40 ml or more. In addition, it is advocated that the patient’s age is 45 years or older.
This is because bleeding in young patients under 45 years of age is often secondary type of cerebral hemorrhage, such as bleeding due to factors such as vascular malformation, aneurysm, and clotting mechanism disorders. For secondary cerebral hemorrhage, blind puncture can bring about secondary injury, which can aggravate the condition. Age is not affected, and the oldest patient I have done is 97 years old. In addition, minimally invasive surgery is usually possible after 6 hours of cerebral hemorrhage onset, and can even be extended to about half a month. In August of this year, I admitted an 87-year-old man who had been in a local hospital for 18 days.
He had a slowly continuing cerebral hemorrhage. The hemorrhage was only 30 ml at the beginning of the episode, and then there were two further hemorrhages, reaching about 80 ml in the basal ganglia area. He was given a minimally invasive surgery on day 18. The patient had a very severe lung infection at that time and was put on a ventilator to assist him in breathing. In the end, this patient was able to walk back, which shows that minimally invasive is very effective and effective for special cases.
8.What kind of neuroprosthetic drugs will be used to improve the prognosis after the cerebral hemorrhage, which can cause secondary cerebral vasospasm after the cerebral hemorrhage has broken into the ventricle?
Cerebral hemorrhage breaking into the ventricles, or primary hemorrhage in the ventricles, as well as subarachnoid hemorrhage can cause secondary inflammatory injury mechanisms due to the toxic effects of blood, which can lead to cerebral vasospasm. Therefore they share a common principle of management, which is to prevent cerebral vasospasm. For example, fasudil and nimodipine are commonly used, and these are drugs that can prevent vasospasm very well. Generally, by preventing or treating vasospasm, patients can be prevented from developing secondary cerebral ischemic injury.
9.Some patients have symptoms of continued bleeding and rebleeding, what are the main causes?
It is easy to find patients with cerebral hemorrhage caused by a ruptured blood vessel. During the process of taking the patient to the hospital emergency room for CT examination, it is possible that the patient continues to bleed. So just 6 hours, or even 12 hours or 24 hours after the bleeding is detected, some patients will continue to bleed and their condition will continue to worsen.
The process of continued bleeding can be very dangerous. Some patients can take a taxi to the emergency room when they first have an attack, but they can’t walk when the doctor examines them and during the CT exam, and they are unconscious after the CT, and they are already in respiratory arrest when they arrive at the hospital room, so the doctor must inform the family, especially the family of a patient who continues to bleed and arrives at the hospital within a short time of the attack, otherwise the family will not understand.
There are many factors that can cause continued bleeding, such as failure to lower excessive blood pressure in a timely manner, the presence of impaired coagulation mechanisms, and the presence of anticoagulants such as aspirin, clopidogrel, and warfarin, which have been taken prior to the onset of the disease. During the course of treatment, the patient’s condition is stabilized, but the patient suddenly becomes more hemiplegic, more unconscious or rapidly falls into a coma, and the patient develops a second bleed, which is called a rebleed. Inadequate treatment management by physicians, such as failure to control persistently very high blood pressure, can cause rebleeding.
In addition, during the recovery period of treatment, as the hematoma is gradually absorbed and the hemoglobin breaks down, the ruptured area is re-exposed. Patients with pre-existing vascular malformations or aneurysms can cause rebleeding when intracranial pressure increases due to laughing, emotional stress, choking, or forceful bowel movements. In addition, if the doctor intervenes surgically without determining whether the patient has a vascular malformation, the puncture needle that enters the brain just in time to puncture the malformed vessel can also cause rebleeding. Rehemorrhage from this cause is also very dangerous. Therefore, for young brain hemorrhage patients under 45 years old, MRA, CTA, or DSA examination should be performed as early as possible to further clarify the diagnosis and avoid secondary factors leading to rehemorrhage.
10.How to prevent some medical complications clinically?
Common complications include secondary pulmonary infections, upper gastrointestinal bleeding, cardiac failure, urinary tract infections, renal impairment, decubitus ulcers, water-electrolyte disturbances, deep vein thrombosis, etc.
Patients who have smoked for a long time or have underlying lung diseases will definitely have a lot of sputum in their lungs once brain hemorrhage occurs. Sputum is a good medium for causing secondary lung infections. For patients with impaired consciousness who are unable to cough up sputum on their own, care should be taken to drain sputum as early as possible with phlegmolytic drugs. If aspiration cannot remove a large amount of sputum, sputum can be sucked out by tracheotomy. In addition, pulmonary infections caused by misaspiration are common.
The patient’s stomach contents enter the lungs due to nausea, vomiting and choking and coughing, causing a lung infection. Therefore, nursing and family members should pump in food slowly when nasal feeding by gastric tube. Also be sure to elevate the patient’s position. It is best to keep the patient’s upper body at a 60-90 degree angle to the bed when playing food, and then adjust it one hour after playing food, keeping the patient’s upper body at a 15-30 degree angle to the bed, which can avoid food residue in the patient’s esophagus.
Complications of upper gastrointestinal bleeding usually occur due to stress ulcers. Stress ulcers are routinely prevented by the use of proton pump inhibitors. In patients with heavy bleeding and thalamic hemorrhage, early intravenous proton pump inhibitors or the addition of gastric mucosal protectors are used to prevent stress ulcers and upper gastrointestinal bleeding.
Heart injury in combination with cerebral hemorrhage is one of the manifestations of cerebro-cardiac syndrome, which mainly includes acute myocardial ischemia, myocardial infarction, cardiac arrhythmia and heart failure. Usually, blood pressure should be controlled first, followed by dehydration agents. Pay attention to the infusion rate and the amount of infusion, and reduce the amount of mannitol by half or switch to other dehydrating agents for elderly patients or patients with pre-existing heart disease. Active treatment of cardiac primary disease is also required.
Urinary tract infections are mainly secondary to urinary incontinence and indwelling catheterization. Therefore, it is important to ensure aseptic operation during catheterization, avoid intubation and indwelling catheterization as much as possible, intermittent catheterization and acidified urine can reduce urinary tract infections, and once they occur, antibiotics should be applied promptly according to bacterial culture and drug sensitivity tests. The most commonly used and classic dehydrating agent, mannitol, has the biggest side effect of damaging renal function. In order to protect renal function, elderly patients should reduce the use of mannitol and instead try to replace it with glycerol fructose or other dehydrating agents.
Decubitus ulcers can be prevented by giving the patient an air mattress, frequent turning, and keeping the skin dry.
Water-electrolyte disorders include hypokalemia, hyponatremia and hypernatremia. Patients should be routinely tested for water and electrolytes and promptly rehydrated to correct them. The patient should also be given nutrients through a gastric tube and nasal feeding.
The inability to move the paralyzed limb and the obstruction of venous return can lead to the formation of venous thrombosis. Patients should be encouraged to move early, lower limbs should be elevated, and lower limb infusion should be avoided (especially on the paralyzed side). Once venous thrombosis occurs anticoagulants should be used, but the use of anticoagulants increases the risk of cerebral rebleeding. Cerebral hemorrhage is a systemic project that requires comprehensive treatment and close attention to changes in the condition on a daily basis.
11.What is the recent progress of cutting-edge research in the treatment of cerebral hemorrhage?
Cerebral hemorrhage is a very complex, very dangerous and challenging disease. In the early stage, we mainly conduct interventions on cerebral hemorrhage, research on minimally invasive and complications. In the later stage, basic research is conducted, focusing on the mechanisms of edema and injury caused by cerebral hemorrhage. He has recently applied for a National Natural Science Foundation of China grant for research related to inflammatory injury mechanisms. Inflammatory injury mechanism is the most common injury mechanism in cerebral hemorrhage. We have explored the toxic response of thrombin, oxygen free radical damage, and gene regulation, which are very popular nowadays, and hope to carry out more in-depth research.