Spontaneous intraventricular hemorrhage

Introduction to spontaneous intraventricular hemorrhage Spontaneous intraventricular hemorrhage refers to intracranial vascular rupture caused by non-traumatic factors, blood enters the ventricular system, and spontaneous intraventricular hemorrhage is divided into two major categories: primary and secondary. Primary intraventricular hemorrhage indicates that blood is derived from the choroid plexus, intraventricular and ventricular wall and paraventricular zone. Secondary intraventricular hemorrhage refers to intraventricular or subarachnoid hemorrhage. Hematoma breaks into or reverses into the ventricle. . basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: upper gastrointestinal bleeding acute renal failure pneumonia

Spontaneous intraventricular hemorrhage

(1) Causes of the disease

It is generally believed that the most common cause of primary intraventricular hemorrhage is choroid plexus aneurysm and cerebral arteriovenous malformation, hypertension and carotid occlusion, moyamoya disease is also a common cause, and other rare or rare causes of intraventricular choroid plexus papilloma Or hamartoma, cyst, bleeding quality, gelatinous cyst or other paraventricular tumor, congenital hydrocephalus, excessive tension, variceal rupture (especially the venous vein or large cerebral vein), subependymal infarction Bleeding, choroid plexus cysticercosis, leukemia, pituitary apoplexy and postoperative (ventral puncture, drainage, shunt), etc., many patients with unknown causes may be related to "hidden hemangioma", using microscope or autopsy detailed examination The choroid plexus may find more "recessive hemangioma".

According to previous literature reports, primary intraventricular hemorrhage with clear etiology classification, aneurysm accounted for the first place, 35.5%; hypertension accounted for the second place, 23.8%; followed by carotid occlusion (including moyamoya disease) accounted for 19.8 %, cerebral arteriovenous malformation accounted for 10.5%, 6.4% for unknown reasons, and 4.1% for other causes.

The cause of secondary intraventricular hemorrhage: hypertension, aneurysm, cerebral arteriovenous malformation, moyamoya disease, intracranial tumor stroke, other rare or rare causes of coagulopathy, accounting for about 0.9% of spontaneous intraventricular hemorrhage, this Part of intraventricular hemorrhage is due to coagulation dysfunction caused by disease, and the other part is the complication of anticoagulant therapy. The diseases causing hemorrhage include leukemia, aplastic anemia, hemophilia, thrombocytopenic purpura, liver disease, and decreased provitamin Symptoms, post-cerebral infarction hemorrhage is another rare cause of secondary intraventricular hemorrhage, accounting for 1.4% of spontaneous intraventricular hemorrhage. Other causes of secondary intraventricular hemorrhage have hemorrhagic constitution, vasospasm after subarachnoid hemorrhage Hemodynamic treatment, systemic lupus erythematosus, cerebral aspergillosis, genetic protein C deficiency, carotid endarterectomy and metabolic disease.

(two) pathogenesis

In the past, many people thought that choroid plexus is the basic source of intraventricular hemorrhage. Hemangioma rupture or rupture of miliary aneurysm can cause primary intraventricular hemorrhage. When the blood vessels differentiate into a diameter of about 3 mm, in the vicinity of the abundant choroid plexus, some Large arteries are anastomosed to the venous endothelium. In these areas, when the original blood vessels are anastomosed, the fistula can occur. Therefore, vascular arteriovenous malformations can occur. Arteriovenous malformations can also occur because the original passage does not disappear. Hemangiomas are defined as limitations. Vascular masses with abnormal number of sexual structures, including normal or malformed arteries and veins and capillaries or a mixture thereof, hemangioma of the paraventricular zone may partially protrude into the ventricles, rupture of hemorrhage may cause primary intraventricular hemorrhage; intraventricular vascular abnormalities It can also occur in the form of deep vascular cystic aneurysm and primary intraventricular hemorrhage, unexplained intraventricular hemorrhage, and recessive hemangioma is considered to be its main source.

Subarachnoid hemorrhage (SAH) or any part of the brain parenchyma may cause secondary intraventricular hemorrhage, because the expansion of the hematoma always proceeds in the direction of least resistance, so the hematoma in the brain parenchyma can penetrate the ventricles. The wall forms intraventricular hemorrhage, and the path of blood from the secondary ventricle into the ventricular system can be divided into two types: countercurrent type and perforation type.

Countercurrent type

For subarachnoid hemorrhage, blood flows back into the ventricular system through the lateral and median holes of the fourth ventricle.

2. Feedthrough type

It is a hematoma in the brain parenchyma or subarachnoid hemorrhage that directly penetrates the ventricle or destroys the brain parenchyma to form a hematoma, and then penetrates the ventricular wall into the ventricular system. This type is divided into five subtypes:

1 lateral ventricle body or triangular area punching type is the most common;

2 lateral ventricle anterior horn penetrating type followed;

3 The third ventricle penetrating type takes the third place;

4 lateral ventricle posterior horn penetrating type is rare;

5 The corpus callosum type is the least seen; the aneurysm ruptures at the Willis arterial ring, and the hematoma can destroy the corpus callosum and enter the third ventricle.

Spontaneous intraventricular hemorrhage prevention

For primary intraventricular hemorrhage, such as due to choroid plexus aneurysm and cerebral arteriovenous malformation, hypertension and carotid occlusion, moyamoya disease and other causes, should actively carry out the cause of treatment to prevent intraventricular hemorrhage.

Spontaneous intraventricular hemorrhage complications Complications upper gastrointestinal bleeding acute renal failure pneumonia

Some patients with spontaneous intraventricular hemorrhage may have complications such as upper gastrointestinal bleeding (21%), acute renal failure (1.2%), and hypostatic pneumonia (25.9%).

Symptoms of spontaneous intraventricular hemorrhage Common symptoms Sensory disturbance Ataxia convulsions Internal convulsions Bleeding medullary hemorrhage Nausea increased intracranial pressure

symptom

The clinical manifestations of spontaneous intraventricular hemorrhage vary in severity. In many cases, the clinical manifestations are benign. The mild cases can only manifest as meningeal irritation without brain localization or disturbance of consciousness, or even manifested as cognitive power such as directional dysfunction without other symptoms. And signs, these patients are often easily misdiagnosed as subarachnoid hemorrhage or missed diagnosis, or intraventricular hemorrhage only found on CT scan, and some patients (15.6%) can self-heal (intraventricular hemorrhage without surgery, Bleeding completely disappears naturally, and the nerve function is completely restored). In severe cases, it is characterized by disturbance of consciousness, convulsion, hemiplegia, aphasia, high fever, high muscle tension, hyperreflexion of the knee, dysfunction of the eye muscles, dilated pupils and bilateral pathological signs. Etc. In the advanced stage, cerebral palsy may occur, and brain rigidity and respiratory circulatory disorders as well as autonomic dysfunction may occur.

Most patients (46.9%) had obvious incentives before onset, the most common (44.7%) were caused by emotional arousal caused by sudden increase in blood pressure, followed by exertive activities (42.1%), bathing (6.1%), drinking (4.4 %) and childbirth (2.6%).

The vast majority (89.3%) of patients with spontaneous intraventricular hemorrhage are acute onset, and a small proportion (10.7%) of patients may have subacute or chronic onset.

The most common first symptoms of spontaneous intraventricular hemorrhage were headache, dizziness, nausea, vomiting (43.2%), followed by disturbance of consciousness (24.7%), hemiplegia (17.7%), aphasia (7%), limb numbness (2.5%). And other symptoms (fever, convulsions, unclear vision, etc.).

Risk factors associated with spontaneous intraventricular hemorrhage include hypertension, heart disease, cerebral infarction, cerebral hemorrhage, and diabetes.

classification

Primary intraventricular hemorrhage

Accounted for 4% to 18% of spontaneous intraventricular hemorrhage, mostly in adolescents or middle-aged, the ratio of male to female is 1:0.86, the clinical manifestations of primary intraventricular hemorrhage, in addition to headache, dizziness, nausea, vomiting, In addition to the general manifestations of elevated blood pressure and meningeal irritation, it has the following characteristics compared with secondary intraventricular hemorrhage:

1 age distribution is polarized, that is, under 30 years old, and over 50 years old is a high incidence age;

2 The disturbance of consciousness is relatively light or absent (76.2%);

3 can be subacute or chronic onset (19%);

4 The positioning signs are not obvious, such as mild or no dyskinesia, less cranial nerve involvement and pupillary abnormalities;

More than 5 cognitive functions (such as memory, attention, orientation and concentration) and mental symptoms are common manifestations.

In addition, intraventricular hemorrhage can occur in upper vision, vasodilation, diabetes insipidus or cortical rigidity, but primary intraventricular hemorrhage can sometimes be dizzy as the only symptom, and no other symptoms and signs, in short, primary Intraventricular hemorrhage is not destroyed by brain parenchyma. If there is no acute obstructive hydrocephalus, the whole clinical process is slower than secondary intraventricular hemorrhage.

2. Secondary intraventricular hemorrhage

Secondary intraventricular hemorrhage accounts for 82% to 96% of spontaneous intraventricular hemorrhage. The original bloodstream of secondary intraventricular hemorrhage is different, and the clinical manifestations are also different.

(1) cerebral hemisphere hemorrhage breaks into the ventricle: cerebral hemisphere hemorrhage breaks into the ventricle, accounting for 84.6% of secondary intraventricular hemorrhage. There are basal ganglia, thalamus and cerebral lobe in the bleeding site. Intraventricular hemorrhage in these areas has general intraventricular hemorrhage. In addition to its characteristics, it also has its own characteristics:

1 basal ganglia hemorrhage into the ventricle: basal ganglia hemorrhage into the ventricle accounted for 4.7% to 33.3% of secondary intraventricular hemorrhage, located in the front of the forearm 2 / 3, especially in the caudate nucleus hematoma, easily broken into the ventricles In this area, 88% to 89.3% of the hematoma penetrated into the lateral ventricle of the lateral ventricle. The clinical manifestations of these patients were often relatively light, the disturbance of consciousness was light, no sensory disturbance, mild hemiplegia, and some patients did not even have obvious brain localization. The hematoma in the 2/3 area of the posterior limb of the internal capsule can be broken through the lateral ventricle triangle or the body is broken into the ventricle, often with a large hematoma, more than 60ml, the condition is generally heavier, due to the relative distance of the hematoma from the ventricle Farther, when the hematoma breaks through the ventricle, the brain parenchyma is severely damaged and the area is large. Therefore, the patient is often characterized by sudden coma, hemiplegia, pathological signs, eyeball gaze to the lesion side, positive for Klinefelter, if the hematoma is in the main hemisphere There is aphasia, respiratory failure and cerebral palsy can occur in severe cases. Hematoma is located in the lower third of the posterior limb of the internal capsule. The hematoma often breaks into the ventricle through the triangle. The patient has sensory disturbances and visual field changes, and the movement disorder is relatively light.

2 thalamic hemorrhage breaks into the ventricle: thalamic hemorrhage into the ventricle accounts for 3.1% to 20.8% of secondary intraventricular hemorrhage, often through the lateral ventricle triangle or body through the ventricle or through the third ventricle into the ventricular system, patients may appear Consciousness disorder, hemiplegia or numbness of the limbs, difficulty in upper eyesight, high fever, diabetes insipidus, positive pathological signs, etc. However, the thalamic hemorrhage in the ventricle is lower than the basal ganglia hemorrhage in the ventricle. Because the thalamic hemorrhage breaks into the ventricle does not necessarily destroy the life center, it can also reduce the pressure on the midline structure of the hematoma, and the thalamic hemorrhage is closer to the ventricle. Even if the ventricle is broken, it will not cause large brain parenchymal destruction, and the thalamic hemorrhage will break. In the ventricles, the amount of hematoma in the brain parenchyma is not necessarily large, averaging about 15.8 ml.

3 cerebral hemorrhage breaks into the ventricle: cerebral hemorrhage breaks into the ventricle and accounts for 1.2% to 8.9% of secondary intraventricular hemorrhage. The clinical manifestations are much more serious than simple cerebral hemorrhage, and the prognosis is also poor. This is because of cerebral hemorrhage. Broken into the ventricles, hematoma needs to destroy a large area of brain parenchyma in order to break through the ventricles, which means that the amount of hematoma is often large, an average of 60ml, up to more than 400ml, such patients are often sudden deep coma, completely hemiplegia, obvious Increased intracranial pressure or cortical rigidity, cerebral palsy and so on.

(2) cerebellar hemorrhage breaks into the ventricle: cerebellar hemorrhage breaks into the fourth ventricle and accounts for 6.4% of secondary intraventricular hemorrhage. If the patient is conscious, he complains of severe headache, dizziness, nausea, vomiting, and back of the neck. Pain, neck rigidity, physical examination showed meningeal irritation positive, ataxia, facial nerve injury, limb paralysis is not obvious, because cerebellar hemorrhage is easy to cause obstructive hydrocephalus, clinical manifestations often rapidly deteriorate and cause disturbance of consciousness; some patients can 1 to 2 hours after the onset of the disease to deep coma, extremity convulsions or rigidity, bilateral pathological signs positive, respiratory failure or sudden respiratory arrest, this part of the patient is often due to massive hemorrhage of the cerebellum, direct compression of the brain stem or cerebellar tonsil Death has occurred.

(3) cerebral bridge hemorrhage breaks into the ventricle: the most common brain stem hemorrhage encountered in the clinic is pons hemorrhage, and pons hemorrhage easily breaks into the fourth ventricle, and brain stem hemorrhage accounts for about 2% of secondary intraventricular hemorrhage. The amount of bleeding is small, the patient can be conscious, have severe headache, vertigo, vomiting, double vision, difficulty swallowing, posterior group of cranial nerve injury, neck stiffness and other manifestations, if a large number of bleeding, patients often tens of minutes or even minutes after the onset It develops into deep coma, high fever, incontinence, acute upper gastrointestinal bleeding, and bilateral diverticulum reduction, cross sputum, respiratory disorders and other signs of vital signs, because this part of the patient is very critical, usually If you do not arrive at the hospital or die in the future, the prognosis is extremely poor and the mortality rate is almost 100%.

(4) Subarachnoid hemorrhage reverses into the ventricle and multiple cerebral hemorrhage breaks into the ventricle:

1 Subarachnoid hemorrhage reverses into the ventricle: Subarachnoid hemorrhage can flow back into the ventricular system through the fourth ventricle, accounting for 5.9% of secondary intraventricular hemorrhage. The clinical manifestations of mild and subarachnoid space without intraventricular hemorrhage Hemorrhage is similar, that is, headache, fever, varying degrees of disturbance of consciousness, mental disorders, epilepsy and cranial nerve palsy, etc., most of the severe cases (92.2%) coma, paroxysmal cortical tonic convulsions, optic disc edema, vitreous hemorrhage, pathology Positive signs, brain localization signs, cerebral palsy and other manifestations, the above-mentioned symptoms and signs are more likely to appear than subarachnoid hemorrhage, and the prognosis is worse than simple subarachnoid hemorrhage.

2 multiple cerebral hemorrhage breaks into the ventricle: multiple cerebral hemorrhage breaks into the ventricle and accounts for 2% of secondary intraventricular hemorrhage. The original bloody part can be divided into cerebral hemisphere and under the curtain. The hemorrhage of the cerebral hemisphere can be the same side. It is a bilateral symmetry site, and there are many blood and curtains under the curtain. The multiple cerebral hemorrhage under the curtain is rare in clinic.

Multiple cerebral hemorrhage breaks into the ventricle. Most patients (80%) have only one sign of hemorrhagic foci or no brain localization. This is mainly related to whether the bleeding site affects the main functional area of the brain, but not with the size of the hematoma. Large, but patients can also have multiple lesions. In addition to the performance of general intraventricular hemorrhage, the clinical process is often heavier. About 80% of patients have disturbance of consciousness and high mortality. It is difficult to diagnose multiple cerebral hemorrhage by clinical manifestation alone. If you break into the ventricles, you must rely on the instrument to help diagnose.

In 1993, according to CT findings and radiological pathological anatomy, Liu Yuguang divided spontaneous intraventricular hemorrhage into five types: type I: hemorrhage was confined to the subependyum, hemorrhage did not break through the ependymal membrane into the ventricular system, and there was no hematoma in the brain parenchyma. Type II: bleeding is limited to the ventricular system, often located in the frontal angle, horn or occipital angle, no hydrocephalus; type III: bleeding is limited to the ventricular system, there may be ventricle cast, and hydrocephalus; type IV: brain Intra-parenchymal hemorrhage breaks into the ventricular system, without hydrocephalus, and is divided into two subtypes, type IVa: hematoma in the supratentorial brain parenchyma <30ml; IVb type: hematoma in the supratentorial parenchyma >30ml or subserosal hematoma; V type: Hematoma in the brain parenchyma breaks into the ventricle, accompanied by hydrocephalus, also divided into two subtypes: Va type: hematoma in the supratentorial brain parenchyma <30ml; Vb type: hematoma in the supratentorial brain parenchyma >30ml or subserosal hematoma.

Spontaneous intraventricular hemorrhage

1. Blood routine, clotting time and prothrombin time

About 85% of cases have white blood cells higher than 1×104/mm3, mainly multinucleated white blood cells, white blood cell counts are mostly (1~2.5)×104/mm3, and hemoglobin may decrease in children. Other routine items may have no obvious changes. The clotting time and prothrombin time are normal in most patients. Only when the cause is leukemia, liver disease, pregnancy-induced hypertension, and anticoagulant therapy, etc., which causes coagulopathy and intraventricular hemorrhage, abnormalities occur. And prothrombin time is prolonged, but sometimes within the normal range.

2. Urine routine

Some patients may have urinary glucose and proteinuria, abnormal blood coagulation or intraventricular hemorrhage caused by pregnancy-induced high eclampsia. Progressive hematuria may occur before and after onset, suggesting that intraventricular hemorrhage may occur.

3. Waist wear check

Almost all patients have bloody cerebrospinal fluid, lumbar puncture pressure more than 2.6kPa (about 200mmH2O), most patients are 3.3 ~ 6.7kPa (250 ~ 500mmH2O), ventricular pressure is 1 ~ 10kPa (80 ~ acute phase of cerebrospinal fluid with red blood cells And neutrophils are predominant, hemosiderin phagocytic cells can be seen 3 to 5 days after the disease, and bilirubin macrophages can be seen in 7 to 10 days. However, this test should be performed cautiously in the acute phase to avoid inducing brain, the waist should be slow when it is discharged, and the amount of liquid should not exceed 8 drops/min and 7ml.

4. Skull flat film

Secondary intraventricular hemorrhage caused by hemispheric hemorrhage can be seen to shift the pineal or choroid plexus calcification plaque to the contralateral side. Because of aneurysms, one side of the iliac crest is enlarged, the internal carotid artery is thickened, and the optic nerve hole is enlarged. Boundary blur, cerebral arteriovenous malformation can be seen in abnormal vascular sulcus, intracranial abnormal calcification spots, intracranial tumor patients can be seen signs of chronic intracranial hypertension, and sometimes partial skull hyperplasia or destruction, the cause of diagnosis of spontaneous intraventricular hemorrhage Have a certain reference value.

5. Cerebral angiography

In addition to the manifestations of spontaneous intraventricular hemorrhage (such as aneurysms, cerebrovascular malformations, moyamoya disease and intracranial tumors) and the manifestations of hematoma in the brain parenchyma, cerebral angiography shows that the hematoma breaks into the ventricle. The lateral membranous artery is displaced to the medial side, and the distal end is compressed or straightened; the anterior cerebral artery is still centered or not displaced, and the internal cerebral vein is obviously displaced to the contralateral side (more than 6 mm) and the anterior cerebral artery There is a phenomenon of "displacement separation", which is a characteristic manifestation of hematoma breaking into the ventricle. The lateral ventricle shows signs of lateral ventricle enlargement, that is, the anterior cerebral artery cerebral artery is spherical and the periorbital artery curvature is increased, the venous angle is enlarged, and the chamber tube is enlarged. Straightening the vein under the membrane.

6.CT scan

CT scan is the safest, most reliable, rapid and non-invasive method for diagnosing intraventricular hemorrhage. If necessary, it should be checked repeatedly to observe its changes dynamically. Intraventricular hemorrhage is characterized by high density in the brain and occasionally as equal density. CT scan can clearly show the location of the original blood, the size of the hematoma, the shape, the degree of cerebral edema, the degree of displacement of the midline structure, the location and extent of hydrocephalus, the extent of the cerebral ventricle and the extent of intraventricular hemorrhage. Etc., provide an important data basis for clinical guidance and treatment to judge prognosis. Repeated CT scan can not only dynamically observe the natural process of hematoma, but also find out whether there is rebleeding.

7.MRI scan

The MRI findings of intraventricular hemorrhage are consistent with the manifestations of cerebral hemorrhage, and the changes in the signal on MRI.

Diagnosis and diagnosis of spontaneous intraventricular hemorrhage

diagnosis

The diagnosis of spontaneous intraventricular hemorrhage, due to the clinical manifestations of spontaneous intraventricular hemorrhage can be light and heavy, vary, CT diagnosis before the diagnosis is based on surgery or autopsy, so the symptoms are often difficult to diagnose or missed diagnosis, misdiagnosis, Any sudden onset, acute intracranial hypertension, disturbance of consciousness, brain location signs, meningeal irritation, etc., should consider the possibility of intraventricular hemorrhage, spontaneous intraventricular hemorrhage by clinical examination to confirm the diagnosis, should be timely Special examinations, especially CT scans and digital subtraction angiography, are necessary to determine the cause. Even so, missed diagnosis may occur because some patients with mild intraventricular hemorrhage may only present with headache, dizziness, and nausea. Vomiting, etc., and unconsciousness or brain positioning signs, so, if there are conditions, the indications for CT scan should be relaxed, and other auxiliary examinations should be performed in time.

Differential diagnosis

Differential diagnosis of the cause of spontaneous intraventricular hemorrhage

1. Hypertensive intraventricular hemorrhage: Most patients with hypertensive intraventricular hemorrhage have a history of obvious hypertension, sudden onset of middle-aged or older, relatively severe disturbance of consciousness, hemiplegia, aphasia more obvious, cerebral angiography without intracranial Aneurysms and malformed blood vessels.

2. Aneurysmal intraventricular hemorrhage: more common in 40 to 50 years old, more women than men, no special symptoms before the onset or one side of the eye muscle paralysis, migraine, etc., the symptoms are serious after the onset, repeated bleeding more common, interval 80 Within 1 month, the patient has a oculomotor nerve injury on one side, progressive vision loss, retinal hemorrhage, and sudden onset of intraventricular hemorrhage on this basis. It is very likely that the aneurysm rupture causes intraventricular hemorrhage. CT scan and cerebral angiography are clearly diagnosed.

3. Cerebral arteriovenous malformation intraventricular hemorrhage: The age of prone to develop is 15 to 40 years old, the average age is about 20 years younger than that of aneurysmal intraventricular hemorrhage. The incidence of gender is opposite to that of aneurysm, that is, males are more than females. History of hemorrhage or epilepsy, progressive hemiparesis without significant increase in intracranial pressure, or posterior fossa symptoms, with slow fluctuations, such as sudden mild disturbance of consciousness and a series of intraventricular hemorrhage, should first consider brain movement Venous malformation, CT scan and cerebral angiography are required for diagnosis.

4. Moyamoya intraventricular hemorrhage: more common in children and young people, before the occurrence of intraventricular hemorrhage, children mainly manifested as paroxysmal hemiplegia, adults mostly showed subarachnoid hemorrhage, on the basis of symptoms and signs of intraventricular hemorrhage Cerebral angiography showed severe stenosis or occlusion of the end of the internal carotid artery, and a dense capillary network at the bottom of the brain, which is characterized by smoke.

5. Intracranial neoplastic intraventricular hemorrhage: more common in adults, where the intraventricular hemorrhage recovery process is not typical or intraventricular hemorrhage in the acute phase of brain edema subsided, the consciousness or positioning signs are not improved, the body found bilateral optic disc edema and other chronic intracranial pressure increased Performance, or the presence of intracranial space-occupying lesions before the onset of the disease or postoperative radiotherapy for patients with brain tumors, should consider the possibility of intracerebral hemorrhage caused by brain tumor hemorrhage, if necessary, CT scan can be confirmed.

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