I. Introduction
Spontaneous intraventricular hemorrhage (Spontanous Intraventricular Hemorrhage) refers to the rupture of intracranial blood vessels due to non-traumatic factors and the entry of blood into the ventricular system.
-Primary Intraventricular Hemorrhage (PIVH) refers to blood originating from the vasculature of the ventricular choroid plexus, intraventricular and paraventricular walls, and paraventricular areas. Primary refers to the pathological manifestation, i.e. the site of hemorrhage, rather than the unknown etiology. Xiao Hui, Department of Neurology, Lianyungang City Hospital of Traditional Chinese Medicine
-According to the vascular anatomy of the centrifugal pathways adjacent to the ventricles and the paraventricular zone, a periventricular hematoma within 1.5 cm from the subventricular canal is also a primary intraventricular hemorrhage.
-Secondary Intraventricular Hemorrhage (SIVH) is defined as intraventricular or subarachnoid hemorrhage in which the hematoma breaks through or refluxes into the ventricles of the brain.
-Spontanous Resolution of Intraventricular Hemorrhage (SRIVH) refers to intraventricular hemorrhage that resolves on its own without surgical treatment and with complete recovery of neurological deficits.
Background
-In 1881, Sanders first classified spontaneous intraventricular hemorrhage into two categories, primary and secondary, based on pathologic data, and described the clinical course of the disease as “sudden coma, brainstem damage, and rapid death.
-Many scholars at home and abroad have discussed this disease in the past, but they were limited to one aspect of the disease, and their findings were affected by the poor diagnostic conditions at that time. Since the clinical application of CT, spontaneous intraventricular hemorrhage can be clearly diagnosed preoperatively, providing an important reference basis for selecting treatment and judging prognosis, and reducing the rate of misdiagnosis and underdiagnosis.
Incidence
-The incidence of spontaneous intraventricular hemorrhage has been reported differently in the literature.
The incidence of spontaneous intraventricular hemorrhage is reported to be 20%-40% in the domestic literature. In the foreign literature, the incidence is 10%-60%.
-Primary intraventricular hemorrhage is generally reported in the literature as 1.96% to 8.6% of spontaneous cerebral hemorrhage, with a mean of 5%; and as 7.4% to 18.9% of intraventricular hemorrhage.
-Spontaneous intraventricular hemorrhage accounts for 13.8% of spontaneous intraventricular hemorrhage.
IV. Etiology
bPrimary intraventricular hemorrhage
-The most common etiologies were choroid plexus aneurysm (35.5%) and cerebral arteriovenous malformation (10.5%).
-Hypertension (23.8%) and carotid occlusion and smog (19.8%) were also common causes.
-Other rare or uncommon causes (4.1%) are intraventricular choroid plexus papillomas or malformations, cysts, hemorrhagic qualities, glial cysts, or other paraventricular tumors.
-Congenital hydrocephalus, hypertension, ruptured varicose veins (especially the thalamic veins or large cerebral veins), infarct hemorrhage in the subventricular space, choroid plexus cysticercosis, leukemia, pituitary stroke, and postoperative (ventriculocentesis, drainage, shunt);
-Many cases of unknown etiology (6.4%) may be associated with “occult hemangiomas”, and detailed examination of the choroid plexus using microscopy or autopsy may reveal more “occult hemangiomas”.
bSecondary intraventricular hemorrhage
-Hypertension (64.3%), aneurysm (19.8%), cerebral arteriovenous malformation (4.2%), smoker’s disease (2.3%), intracranial tumor stroke (1.0%).
-Rare causes include coagulation abnormalities (0.9% ) and post-infarction hemorrhage ( 1.4% )
C coagulation disorders Leukemia, aplastic anemia, hemophilia, thrombocytopenic purpura, liver disease, and vitaminogen hypoplasia
C Complications of anticoagulant therapy
-Other rare causes
C alcoholism (Weisberg , 6 cases , 1988)
C melancholia (Yoshioka , 3 cases, 1981 )
C ruptured hemorrhage from fungal aneurysm and ruptured hemorrhage from cerebellar arteritis (Little, 3 cases and 1 case, 1977)
C eclampsia (Mizobuchi, 1 case, 1988; Liu Yuguang, 2 cases, 1990)
C others with hemorrhagic body, hemodynamic treatment of vasospasm after subarachnoid hemorrhage, systemic lupus erythematosus, cerebral varicose disease, genetic protein C deficiency, post carotid endarterectomy and metabolic diseases.
V. Pathological basis and pathogenesis
bMany previously considered the choroid plexus to be the underlying source of intraventricular hemorrhage.
bRupture of a vascular malformation or rupture of a cornu aneurysm can cause primary intraventricular hemorrhage.
bAneurysms in the paraventricular zone can partially protrude into the ventricles and rupture and bleed causing primary intraventricular hemorrhage.
bIntraventricular vascular abnormalities can also occur in the form of deep vascular cystic aneurysms and cause primary intraventricular hemorrhage.
bInsidious intraventricular hemorrhage of unknown origin, with occult hemangioma considered to be the main source.
bSubarachnoid hemorrhage or hemorrhage anywhere in the brain parenchyma may cause secondary intraventricular hemorrhage.
bThe expansion of the hematoma always proceeds in the direction of least resistance, so the hematoma in the brain parenchyma can penetrate the ventricular wall to form an intraventricular hemorrhage.
bThe pathways by which blood exiting secondary intraventricular ventricles enters the ventricular system can be divided into two types: the countercurrent type and the penetrating type.
bReflux type Blood enters the ventricular system through the lateral and median foramina of the fourth ventricle after subarachnoid hemorrhage.
b Penetrating type A hematoma in the brain parenchyma or subarachnoid hemorrhage directly penetrates the ventricle or destroys the brain parenchyma to form a hematoma, which then penetrates the ventricular wall and enters the ventricular system.
-The lateral ventricular body or triangle penetration type is the most common;
-Lateral ventricular anterior horn penetration, the second most common type;
-Third ventricular penetration, which is the third most common;
-Passage through the posterior horn of the lateral ventricle, which is rare;
-The rupture of aneurysm at the ring of Willis artery and hematoma can destroy the mouth of corpus callosum and enter the third ventricle.
VI. Clinical manifestations
bThe clinical manifestations of spontaneous intraventricular hemorrhage vary in severity, and in many cases the clinical manifestations are benign in course.
bMild cases may only show signs of meningeal irritation without brain localization signs or impaired consciousness, or even only cognitive dysfunction such as orientation without other symptoms and signs.
bThese patients are often easily misdiagnosed as subarachnoid hemorrhage or missed, or intraventricular hemorrhage is only detected on CT scan, and some patients can heal spontaneously.
bSevere cases present with impaired consciousness, twitching, hemiparesis, aphasia, hyperthermia, hypertonia, hyperactive knee reflexes, impaired eye muscle movement, narrow pupils and positive bilateral pathological signs.
bLater, brain herniation, denervation and respiratory and circulatory disorders as well as vegetative neurological disorders may occur.
bSome patients may have upper gastrointestinal bleeding (21%), acute renal failure (1.2%), and pneumonic pneumonia (25.9%).
b Sex and age The ratio of male to female is 1:0.75; it can occur at any age, and those aged 41-70 years are the most common age, accounting for 73.7% of the total.
The shortest duration of illness was 10 minutes, and the longest was 30 days, with an average of 3.1 days. The duration of the disease was within 1 day in 55.l% of the cases.
bCauses 46.9% had obvious causes before the onset of the disease.
-The most common trigger (44.7%) was a sudden increase in blood pressure due to emotional stress.
-This was followed by vigorous activity (42.1%), bathing (6.1%), alcohol consumption (4.4%), and childbirth (2.6%).
bMode of onset: 89.3% of patients with spontaneous intraventricular hemorrhage have an acute onset, while 10.7% may have a subacute or chronic onset.
bRisk factors
-hypertension (71.5%)
-Heart disease (8.9%)
-History of cerebral infarction (8.8)
-History of cerebral hemorrhage (2.8%)
-Diabetes mellitus (1.6%)
bFirst symptoms
-Headache, dizziness, nausea, vomiting (43.2%)
-Disorders of consciousness (24.7%)
-Heparesis (17.7%)
-Aphasia (7%)
-Numbness of limbs (2.5%)
-Other symptoms (fever, paralysis, blurred vision, etc.)
bCharacteristics of primary intracerebral hemorrhage
-Bipolar age distribution, i.e. under 30 years of age and over 50 years of age as the high incidence age;
-Relatively mild or absent impairment of consciousness (76.2%);
-Can be subacute or chronic in onset (19%);
-Localization signs are not obvious, such as mild or no motor disturbances, less frequent cranial nerve involvement and pupillary abnormalities;
-Cognitive impairment (e.g., memory, attention, orientation, and concentration) and psychiatric symptoms are the most common manifestations.
bCharacteristics of secondary intraventricular hemorrhage
-hemorrhage in the cerebral hemispheres being into the ventricles Hemorrhage in the cerebral hemispheres breaking into the ventricles accounts for about 84.6% of secondary intraventricular hemorrhage. The sites of hemorrhage include the basal ganglia, thalamus, and lobes. In addition to the characteristics of general intraventricular hemorrhage, intraventricular hemorrhage in these sites has its own characteristics.
Basal ganglia hemorrhage into the ventricle
C thalamic hemorrhage into the ventricle
C Lobar hemorrhage into the ventricle
b Basal ganglia hemorrhage breaking into the ventricle Basal ganglia hemorrhage breaking into the ventricle accounts for about 4.7%-33.3% of secondary intraventricular hemorrhage.
-Hematomas located in the anterior 2/3 of the anterior limb of the internal capsule, especially in the caudate nucleus, are highly susceptible to rupture into the ventricles, and approximately 88% to 89.3% of hematomas in this area penetrate the anterior horn of the lateral ventricles and rupture into the lateral ventricles.
-The clinical manifestations of such patients are often relatively mild, with mild impairment of consciousness, no sensory impairment, mild hemiparesis, and some patients even have no obvious brain localization signs.
-The hematoma in the anterior 2/3 region of the posterior limb of the internal capsule may penetrate the lateral ventricular triangle or the body and break into the ventricles, often with a larger hematoma, mostly above 60 ml, and the condition is generally more severe.
-Because of the relative distance of the hematoma from the ventricle, when the hematoma penetrates the ventricle, the brain parenchyma is severely damaged and the area is large, so the patient mostly shows sudden coma, hemiparesis, positive pathological signs, eye gazing to the side of the lesion, positive Kirsch’s sign, and there may be aphasia if the hematoma is in the main hemisphere.
-In severe cases, respiratory failure and brain herniation may occur.
-In hematomas located in the posterior l/3 of the posterior limb of the internal capsule, the hematoma often breaks into the ventricle through the triangle, and the patient mostly has sensory disturbances and visual field changes, while motor disturbances are relatively mild.
b Thalamic hemorrhage into the ventricle
Thalamic hemorrhage into the ventricle accounts for about 3.1%-20.8% of secondary intraventricular hemorrhage, often penetrating the ventricle through the lateral ventricular triangle or the body or penetrating the three ventricles into the ventricular system.
-Patients may present with impaired consciousness, hemiparesis or limb numbness, difficulty in upward vision of both eyes, high fever, uveitis, and positive pathological signs.
-Thalamic hemorrhage that penetrates the ventricles has a lower mortality rate than basal ganglia hemorrhage that penetrates the ventricles.
-This is because a thalamic hemorrhage that penetrates the ventricle does not necessarily destroy the vital center; it also reduces the compression of midline structures by the hematoma, and because the thalamic hemorrhage is closer to the ventricle, even if it penetrates the ventricle, it does not cause extensive destruction of brain parenchyma.
-When thalamic hemorrhage breaks into the ventricle, the amount of hematoma in its brain parenchyma is not necessarily large, averaging about 15.8 ml.
bLobar hemorrhage into the ventricle
-Lobar hemorrhage breaking into the ventricles accounts for about 1.2% to 8.9% of secondary intraventricular hemorrhage. Its clinical manifestations are much more severe than those of lobar hemorrhage alone, and the prognosis is poor.
-This is because when lobar hemorrhage breaks into the ventricles, the hematoma needs to destroy a large area of brain parenchyma in order to penetrate the ventricles, which means that the hematoma volume is often large, averaging 60 ml and reaching a maximum of 400 ml or more.
-This means that the hematoma volume is often very large, averaging 60 ml and up to 400 ml or more. Such patients mostly present with sudden deep coma, complete hemiparesis, marked increase in intracranial pressure or decerebrate brain tonicity, and brain herniation.
b Cerebellar hemorrhage into the ventricle
-Cerebellar hemorrhage into the fourth ventricle accounts for about 6.4% of secondary intraventricular hemorrhage, and most of them have acute onset.
-If the patient is clear, he mostly complains of severe headache, dizziness, nausea, vomiting, posterior neck pain, cervical ankylosis, and positive meningeal stimulation signs, ataxia, and facial nerve injury are seen on physical examination. Limb paralysis is not obvious.
-As cerebellar hemorrhage tends to cause obstructive hydrocephalus, the clinical manifestations often deteriorate rapidly and result in impaired consciousness;
-Some patients may develop deep coma, twitching or tonicity of the limbs, positive bilateral pathological signs, respiratory failure or sudden respiratory arrest within 1-2 hours after the onset of the disease.
-These patients often die due to massive cerebellar hemorrhage, which directly compresses the brainstem or causes submural herniation of the cerebellum.
bPontocerebral hemorrhage breaking into the ventricles of the brain
-The vast majority of brainstem hemorrhages encountered clinically are pontocerebral hemorrhages, and pontocerebral hemorrhages tend to break into the fourth ventricle.
-Brainstem hemorrhage accounts for approximately 2% of secondary intraventricular hemorrhages. If the hemorrhage is small, the patient may be conscious, with severe headache, blurred vision, vomiting, diplopia, dysphagia, posterior group cranial nerve injury, and cervical ankylosis.
-In case of massive bleeding, the patient often develops deep coma, high fever, urinary and fecal incontinence, acute upper gastrointestinal hemorrhage, and other symptoms such as bilateral pupil narrowing, crossed paralysis, and respiratory disturbance within minutes after the onset of bleeding.
-The prognosis is very poor and the mortality rate is almost 100% because these patients are very critical at the onset and often die before they reach the hospital or have time to be treated.
bSubarachnoid hemorrhage into the ventricles
-Subarachnoid hemorrhage can flow back into the ventricular system through the fourth ventricle, accounting for about 5.9% of secondary intraventricular hemorrhage.
-In mild cases, the clinical presentation is similar to that of subarachnoid hemorrhage without intraventricular hemorrhage, i.e., headache, fever, varying degrees of impaired consciousness, psychiatric abnormalities, epilepsy, and cranial nerve palsies.
-The majority (92.2%) of the severe cases presented with coma, episodic denervation tonic convulsions, optic papilloedema, subvitreous hemorrhage, positive pathological signs, cerebral localization signs, and brain herniation.
-These signs and symptoms are much more likely to occur than in subarachnoid hemorrhage alone, and the prognosis is worse than in subarachnoid hemorrhage alone.
bPolycystic hemorrhage into the ventricles
-Multiple cerebral hemorrhages into the ventricles account for approximately 2% of SIVH.
-This is mainly related to whether the site of hemorrhage affects a major functional area of the brain, but not to the size of the hematoma.
-Patients may also present with multifocal manifestations, and in addition to having the usual manifestations of intraventricular hemorrhage, often have a more severe clinical course, with approximately 80% of patients presenting with impaired consciousness and high mortality.
-It is difficult to diagnose multiple cerebral hemorrhages breaking into the ventricles by clinical manifestations alone.
VII. Diagnosis and etiological differential diagnosis
bDiagnosis of spontaneous intraventricular hemorrhage can be mild or severe due to its clinical manifestations, which vary. Before the introduction of CT, the definite diagnosis was mostly based on surgery or autopsy, and it is often difficult to diagnose or miss or misdiagnose the in vivo preoperative cases or those with mild symptoms.
b Anyone with sudden onset, acute intracranial pressure increase, impaired consciousness, cerebral localization signs, meningeal irritation signs and other manifestations should be considered to have intraventricular hemorrhage.
bSpontaneous intraventricular hemorrhage is difficult to be diagnosed by clinical examination alone, and special examinations, especially CT scan and digital subtraction cerebral angiography, should be performed in a timely manner, which is necessary to clarify the cause.
b Even so, the diagnosis can be missed because some patients with mild intraventricular hemorrhage may only present with headache, dizziness, nausea and vomiting, without consciousness impairment or brain localization signs.
bThe indications for CT scan should be relaxed, and special auxiliary examinations should be performed promptly.
bSpecial examinations
-Ventriculography
C-ventricular enlargement;
C-ventricular deformation and displacement;
C-ventricular filling defect, a characteristic sign of spontaneous intraventricular hemorrhage;
Enlarged or non-visible C-ventricular pools and sulci;
C-ventricular pool filling defect.
b Cerebral angiography
-shows the etiology of spontaneous intraventricular hemorrhage
-Demonstration of intracerebral parenchymal hematoma
-Hematoma breaking into the ventricles fashioned as.
C-anterior view shows medial displacement of the lateral ductus arteriosus, with distal compression or straightening; the anterior cerebral artery remains centered or is not significantly displaced, while the internal cerebral vein is significantly displaced to the opposite side (more than 6 mm) with “displacement separation” between the anterior cerebral artery, which is characteristic of a hematoma breaking into the ventricle.
The lateral ventricular enlargement is seen in C-slide film, i.e. spherical shape of the knee of the anterior cerebral artery and increased curvature of the pericallosal artery, larger venous angle, and straightening of the subventricular vein.
bCT scan
CT scan is currently the safest, most reliable, rapid and non-invasive means of diagnosing intraventricular hemorrhage.
-Repeated examinations should be performed when necessary to allow dynamic observation of changes.
Intraventricular hemorrhage may appear as a high-density intracerebroventricular shadow, or occasionally as an isointensity shadow.
-CT scan can also clearly show the site of primary hemorrhage, the size and shape of the hematoma, the degree of cerebral edema, the degree of displacement of midline structures, the site of hydrocephalus obstruction and its degree, the site of ventricular penetration and the degree of intraventricular hemorrhage, etc., which provide important information for clinical guidance of treatment and prognosis.
-Repeated CT scans can not only dynamically observe the natural course of the hematoma, but also detect whether there is rebleeding.
bMRI Its MRI performance is consistent with that of cerebral hemorrhage
bEtiology differential diagnosis
-hypertensive intracerebral hemorrhage
C The majority have a significant history of hypertension;
C sudden onset in middle age or older;
C Consciousness impairment is relatively severe;
C hemiplegia and aphasia were more pronounced;
The cerebral angiogram was free of intracranial aneurysms and malformed vessels.
-Aneurysmal intracerebral hemorrhage
C Most commonly seen in 40-50 years old;
C more females than males
C No specific symptoms before onset or one side of the eye muscle paralysis, migraine, etc.
The symptoms are severe after the onset of the disease, and repeated bleeding is more common, with an interval of 80% within 1 week.
The sudden appearance of intraventricular hemorrhage on the basis of arteriovenous nerve damage, progressive vision loss and retinal hemorrhage on one side of C is likely to be caused by ruptured aneurysm hemorrhage, and CT scan and cerebral angiography should be performed promptly to clarify the diagnosis.
-Cerebral arteriovenous malformation intraventricular hemorrhage
The age of C is 15-40 years old, and the average age is about 20 years younger than that of aneurysmal intraventricular hemorrhage.
The incidence of C by gender is opposite to that of aneurysm, i.e., more males than females.
C may have a history of hemorrhage or epilepsy before onset, progressive mild hemiparesis without obvious manifestations of increased intracranial pressure, or posterior cranial fossa symptoms with a slow fluctuating progression.
If C suddenly occurs with mild impaired consciousness and a series of intraventricular hemorrhagic manifestations, cerebral arteriovenous malformation should be considered first.
CConfirmation of the diagnosis requires CT scan and cerebral angiography.
-Smoldering intraventricular hemorrhage
C is usually seen in children and young adults
Before the onset of intraventricular hemorrhage, children mainly present with episodic hemiparesis, while adults present with subarachnoid hemorrhage, on which the signs and symptoms of intraventricular hemorrhage appear
C Cerebral angiography shows severe stenosis or occlusion of the end of the internal carotid artery, with a dense capillary network at the base of the brain, which is characterized by a smoke-like appearance.
-Intracranial tumor intraventricular hemorrhage
C Most commonly seen in adults
If the recovery process of intraventricular hemorrhage is atypical or the cerebral edema in the acute phase of intraventricular hemorrhage has subsided, and the mental or localization signs do not improve, and chronic intracranial pressure increase such as bilateral optic nerve papillary edema is found on physical examination, or patients with intracranial occupying lesions before the onset or postoperative radiotherapy for brain tumor, the possibility of intraventricular hemorrhage due to brain tumor hemorrhage should be considered.
CT-enhanced scan is feasible to confirm the diagnosis if necessary.
-Intraventricular hemorrhage of other rare or uncommon etiologies
Most of them have an obvious etiology, and it is not difficult to make the etiological diagnosis based on the medical history.
Hematologic disease
Anticoagulation therapy
C alcoholism
C melancholia
C fungal aneurysm and cerebellar arteritis
C Eclampsia
Classification and typing
bSanders’ classification (1881)
-Sanders was the first to classify intraventricular hemorrhage into two categories, primary and secondary, according to the site of primary hemorrhage based on autopsy data. Although this classification is rather general, it is the most basic and commonly used classification method.
bLittle typing method (1977)
-Intraventricular hemorrhage is classified into three types according to clinical and CT manifestations
VIII. Classification and typing
-Type I: CT shows massive intraventricular hemorrhage, usually filling the entire ventricular system or pontocerebral hemorrhage breaking into the third and fourth ventricles, characterized by sudden onset, deep coma, and brainstem damage, with death mostly within 24 hours.
-Type II: CT scan shows a large hematoma in the brain parenchyma and rupture into the ventricles. The extent of intraventricular hemorrhage is smaller than that of type I. The clinical presentation is characterized by sudden onset, impaired consciousness, and signs of brain localization, but it is milder than that of type I patients. Patients who survive this type often have severe sequelae.
-Type III: CT shows a more limited intracerebroventricular hematoma with a relatively small parenchymal hematoma. Patients present clinically with an acute onset, with cerebral localization signs or with sudden severe headache, lethargy, confusion, and no neurological localization signs.
-The mortality rates for these three types are 100%, 87.5% and 15%, respectively.
-Little’s staging method has more comprehensively combined clinical and CT to comprehensively evaluate the prognosis of intraventricular hemorrhage, but this staging method is clearly not applicable to those whose clinical presentation is inconsistent with CT presentation.
bFenichel grading method (1980)
-Grade I: Simple subventricular hemorrhage;
-Grade II: intraventricular hemorrhage without ventricular dilatation;
-Grade III: intraventricular hemorrhage with ventricular dilatation;
-Grade IV: intraventricular hemorrhage with ventricular dilatation and parenchymal hemorrhage.
-Grading is consistent with survival, i.e., grade I has the highest survival rate and grade IV has the worst prognosis.
bGraeb score grading (1982)
-Graeb score grading method.
The total score was 12, with 1-4 being mild intraventricular hemorrhage, 5-8 being moderate, and 9-12 being severe.
-The mortality rates for the three levels were 32.3%, 57.7% and 99%, i.e., the higher the score, the higher the mortality rate.
-But Graeb’s grading study did not exclude the prognostic impact of factors such as intracerebral parenchymal hematoma on intraventricular hemorrhage.
bVerma score grading method (1987)
-Verma score grading method.
C total score of 10 , 1 to 3 for mild, 4 to 7 for moderate, and 8 to 10 for severe.
CVerma grading method then excluded the prognostic effect of intracerebral parenchymal hematoma, i.e., cases with intracerebral parenchymal hematoma less than 5 ml were selected for the study, and it was found that mild intracerebral hemorrhage with a score less than 3 had a mortality rate of 50%; while moderate to severe with a score of 4 to 10 had a mortality rate of 46.3%.
C Therefore, he concluded that the amount of intracerebroventricular hemorrhage was not closely related to the prognosis.
b Fang Yannan Classification (1988) classified intraventricular hemorrhage into small, medium and large intraventricular hemorrhage according to the extent of intraventricular distribution of high-density shadow on CT.
-Small amount: Intraventricular hyperintensity shadow is less than 1/3 of the ventricular area;
-Medium amount: l/3 to 1/2 of the ventricular area;
-Large amount: more than 1/2 of the intracerebroventricular area.
b Liu Yuguang grading method (1991) combines clinical and CT, overcomes the shortcomings of the above grading method, and selects the indicators closely related to prognosis for grading.
-Total score of 20 points, 0~5 is grade I, 6~10 is grade II, 11~15 is grade III, 16~20 is grade IV.
-The higher the grade, the higher the mortality rate.
b Liu Yuguang CT typing method (1993) proposed a CT five-type classification of spontaneous intraventricular hemorrhage based on CT performance and radiological pathological anatomy.
-Type I: The hemorrhage is confined to the subventricular canal, the hemorrhage does not penetrate the ventricular canal into the ventricular system, and there is no hematoma in the brain parenchyma;
-Type II: The hemorrhage is limited to the localized ventricular system, often located in the frontal, temporal or occipital horn, and there is no hydrocephalus;
-Type III: hemorrhage confined to the ventricular system, may have ventricular casts, and hydrocephalus;
Type-IV: hemorrhage in the brain parenchyma breaks into the ventricular system without hydrocephalus. It is further divided into two subtypes
Type CIVa: supratentorial hematoma less than 30 ml;
Type CⅣb: supratentorial hematoma greater than 30 ml or subatrial hematoma;
-Type V: intracerebral parenchymal hematoma breaking into the ventricles with hydrocephalus; also divided into two subtypes
Type CVa: supratentorial hematoma less than 30ml;
Type CVb: supratentorial parenchymal hematoma greater than 30ml or subscriptive hematoma.
IX. CT performance
bIt is generally believed that CT shows a high-density shadow of the hematoma, which can be confirmed at least 1 hour after the onset.
bThe time of CT examination for spontaneous intracerebral hemorrhage should be 1 hour to 2 weeks after onset;
b100% positive in 1 to 2 weeks, 50% positive in 3 to 4 weeks, and after 4 weeks, the blood is absorbed and the density of intracerebroventricular hematoma is the same as that of cerebrospinal fluid.
bCT manifestation of intraventricular hemorrhage is overwhelmingly a high-density intracerebroventricular shadow, but it can also manifest as an isointensity shadow.
bCT era, the incidence of intraventricular hemorrhage is reported in the literature to account for 26%-60% of spontaneous cerebral hemorrhage.
Diagnostic criteria for bCT
-The cerebrospinal fluid must be dense with blood or clots to be seen visually on CT as denser than the surrounding brain tissue (New, 1976).
-The erythrocyte ratio in the cerebrospinal fluid is above 16% to show up on CT, while below 12% the CT value of the cerebrospinal fluid does not change significantly and cannot be shown on CT (Scott, 1974).
-The detection rate of CT is not 100%, so the failure to detect intracerebroventricular hemorrhage on CT does not absolutely exclude the disease.
bThe intraventricular hemorrhage can be distinguished on CT as intracerebroventricular clot or bloody cerebrospinal fluid.
b Although both show intracerebroventricular hyperdensity on CT, the CT value of a fresh clot is between +40 and +80 Heinz units, whereas that of a bloody cerebrospinal fluid is between +20 and +40 Heinz units.
bThe morphology of intracerebroventricular hematoma can be classified as punctate, fluid flat, and cast, while the cerebrospinal fluid-blood mixture is usually seen in the occipital horn on CT, and a “fluid flat shadow” between high-density or high-low-density shadow in the occipital horn is common on scan.
b Intracerebroventricular hematoma volume
-Because intracerebroventricular hematoma is irregular and varies in shape, it is difficult to accurately calculate the amount of hematoma based on CT.
-Most scholars classify intraventricular hematoma as small, medium, or large intraventricular hemorrhage according to the amount of intraventricular hematoma occupying the ventricles.
CSmall intraventricular hemorrhage Less than l/3 of the area of the ventricular system
C moderate intraventricular hemorrhage 2/3 of the area of the ventricular system
C massive intraventricular hemorrhage More than 2/3 of the area of the ventricular system
B Site of ventricular penetration In secondary intraventricular hemorrhage, the site of ventricular penetration by intracerebral parenchymal hematoma can be classified as:
Anterior horn of the C lateral ventricle (26.7%)
C lateral ventricular body (30.2%)
C lateral ventricular triangle (18.3%)
C posterior horn of the lateral ventricle (3.0%)
C third ventricle (5.9%)
C fourth ventricle (8.4%)
C unknown site (7.4%)
b occlusive hematoma
-Blood entering the ventricles is classified into occlusive and non-occlusive hematomas on CT depending on whether the intraventricular hematoma fills the interventricular foramen, aqueduct, and the third and fourth ventricles.
-The incidence of occlusive hematomas in intraventricular hemorrhage ranges from 34.6% to 51.6%.
-The incidence of occlusive hematoma with acute obstructive hydrocephalus was 73.9%.
-In addition to obstructing the cerebrospinal fluid circulation and causing hydrocephalus, occlusive hematomas also directly compress the midline structures and the third and fourth ventricles, resulting in high mortality.
b Ventricular cast
-There is no strict definition of ventriculocasts, but they are generally defined as hematomas that fill the entire ventricle on CT.
-The incidence of ventricular casts is approximately 21.9%.
-Ventricular casts are classified as lateral ventricular casts on one side, bilateral lateral ventricular casts, third ventricular casts, fourth ventricular casts, and whole ventricular casts.
-The whole ventricular system cast was rare, accounting for only 6.1%.
bCT follow-up Repeated CT review or regular CT follow-up not only allows dynamic observation of the natural course of the hematoma, but also detects whether there is rebleeding or secondary changes after hemorrhage and posterior CT manifestations after the hematoma has resolved.
-Intracerebroventricular hematoma
CIt is generally believed that intracerebroventricular hematomas disappear more quickly by natural resorption than do parenchymal hematomas.
CThis may be related to the production and absorption of cerebrospinal fluid and the continuous dilution and dissolution of the hematoma.
C Watanabe (1986) reported that a small amount of intraventricular hemorrhage could resolve after 1 week.
CLittle (1977) reported a high-density intracerebroventricular hematoma that was found to gradually decrease in density with multiple reexaminations of CT, decreasing to normal cerebrospinal fluid density (+1 to +5 Heinz units) in an average of 12 days.
The absorption of hematoma is slower in C-ventricular casts, and some of them even take 3 months to be absorbed, which may be related to the obstruction of cerebrospinal fluid circulation and the lack of dilution and dissolution of hematoma.
C Liu Yuguang et al. (1991) reported
C The general intracerebroventricular hematoma disappears in 4 to 27 days, with an average of 14.6 days.
The rate of decrease in CT values for C intracerebroventricular hemorrhage was 0.8 to 4.0 Heinz units/day, with a mean of 2.4 Heinz units/day.
The sequence of intracerebral hematoma disappearance in C ventricle was fourth ventricle, third ventricle and lateral ventricle in that order.
The vast majority of brains in C survival cases.