Intraventricular hemorrhage

Introduction The ventricle is a cavity in the brain, and there is a lateral ventricle in the cerebral hemisphere. The sagittal fissure between the thalamus and the hypothalamus is called the third ventricle. The fourth ventricle is between Yannao, Qiao and Cerebellum. There are small holes in each ventricle. Ventricular hemorrhage refers to bleeding in these compartments. Divided into primary and secondary. The rupture of the choroidal artery on the ventricular wall is called primary ventricular hemorrhage, which is relatively rare. Hemorrhage in the brain parenchyma is broken into the ventricle and is called secondary ventricular hemorrhage. This type of bleeding is more common. In clinical practice, in addition to the general manifestations of cerebral hemorrhage, ventricular hemorrhage often has some special manifestations, which are signs that the blood breaks into the ventricles.

Cause

The incidence of primary intraventricular hemorrhage accounts for 3.1% to 8.6% of cerebral hemorrhage [1], and the mortality rate is 46%. Usually the disease is caused by rupture of ventricular wall vascular malformation, hypertension microaneurysm, choroid plexus aneurysm, rare causes are: brain tumor, bleeding quality, venous rupture, congenital hydrocephalus. In addition, for unknown reasons, many people think of occult vascular disease.

The pathogenesis of PIVH is closely related to the characteristics of blood supply to the ventricular wall. According to the study of blood supply to the ventricle near the ventricle, the wall blood vessels from the anterior and posterior choroidal arteries and the bean-like arteries are radially distributed to the white matter and the deep nerve gray matter nuclei in the 1.5cm range near the ventricle. The parenchymal blood vessels supply concentricity to the deep part of the blood. At the 1.5cm side of the ventricle, the two groups of blood vessels form a watershed. These blood vessels are terminal arterioles, which do not coincide with each other and have poor collateral circulation. Therefore, this area is highly susceptible. Ischemic damage. In addition, these blood vessels form a vascular network under the ependymal membrane, and their distal ends are dilated and prone to bleeding.

an examination

Related inspection

Fall test CT scan of the brain

(1) lateral ventricle and third ventricle hemorrhage

1 rapid onset, rapid deep coma, a small number of conscious.

2 vomiting, hematemesis.

3 bilateral pathological reflexes appear.

4 The muscle tension of the limbs is increased, and there is periodic spontaneous muscle tension in the early stage. When the brain is paralyzed or the brain is strong, the limbs become flaccid.

5 bilateral pupil reduction, eyeball floating, separation strabismus.

6 often have hypothalamic lesions, showing elevated body temperature, heart rate, pulse slow and fast, facial congestion and sweating, blood sugar and white blood cells increased. Early pulmonary edema and changes in respiratory rhythm and frequency.

7 cerebrospinal fluid pressure is high, bloody.

(2) fourth ventricle hemorrhage

Often caused by brain stem or cerebellar hemorrhage secondary to the fourth ventricle, damage to the medullary life center, it often died within a few hours. In the short time of survival, the following performance can be achieved:

1 In the early stage of the disease, the disturbance of consciousness was lighter, and then developed rapidly into a deep coma.

2 vomiting, hiccups, sputum reflexes disappeared, pathological reflexes.

3 high fever, body temperature often reaches 40 ° C or more.

4 No reflexive or spontaneous hyperactivity, no groping and pointing action.

5 The vestibular reflex disappears.

6 early pulmonary edema and respiratory disorders.

7 heartbeat slows, irregular rhythm, blood pressure drops.

8 cerebrospinal fluid is bloody.

Differential diagnosis

Differential diagnosis

Thalamic hemorrhage: obstructive hydrocephalus is prone to occur after thalamic hemorrhage breaks into the ventricles. Thalamic hemorrhage caused obstructive hydrocephalus, the patient was comatose at the time of onset, relieved after conservative treatment of internal medicine, obstruction was relieved, and consciousness was restored. Coma at the time of onset leads to death. The amount of thalamic hemorrhage broke into the ventricles, and there were 23 cases with more than 15ml, indicating that the greater the amount of bleeding, the greater the possibility of breaking into the ventricles.

Bridge cerebral hemorrhage: about 10% of cerebral hemorrhage, mostly caused by rupture of the pons of the basilar artery. Clinical manifestations include sudden headache, vomiting, dizziness, diplopia, different axes of the eye, side palsy, cross sputum or hemiplegia, quadriplegia. When the amount of bleeding is small, the patient's consciousness can be expressed as some typical syndromes, such as foville syndrome, millard-gubler syndrome, atresia syndrome, etc., may be accompanied by high fever, sweating, stress ulcers, acute pulmonary edema, Acute myocardial ischemia and even myocardial infarction. When a large amount of hemorrhage occurs, the hematoma spreads to both sides of the pons and the covered part of the pons. The patient quickly enters a coma. The bilateral pupils are needle-like, side-viewing paralysis, quadriplegia, difficulty breathing, and have a brain-strength attack. They can also vomit brown stomach contents. There are midline symptoms such as central hyperthermia, often dying within 48 hours.

Deep hemorrhage of the brain parenchyma: Hypertensive cerebral hemorrhage occurs mostly in the deep arterioles of the brain. Hypertensive cerebral hemorrhage is one of the most serious complications of hypertension. The incidence rate of males is slightly higher, which is more common in elderly people aged 50-60 years, but it can also occur in young hypertensive patients. The clinical features are sudden and severe headaches, and often accompanied by convulsions, lethargy or coma. Hemiplegia and pupillary changes occurred on the contralateral side of the hematoma, and the pupils on both sides were narrowed at the early stage. When the hematoma expanded, the cerebral edema aggravated, the intracranial pressure increased, the cerebral palsy caused by the dilated pupils on the hematoma side, respiratory disorders, and pulse slowed down. ,High blood pressure. Then it turned into central failure. Cerebellar hemorrhage: refers to bleeding in the parenchyma of the cerebellum, which is directly related to hypertension. Most of the sudden onset of symptoms of dizziness, frequent vomiting, occipital headache, one side of the upper and lower limbs ataxia without obvious paralysis, may have nystagmus, one side of the facial paralysis. A small number of subacute progressive, similar to cerebellar space-occupying lesions. Severe massive hemorrhage showed rapid progressive intracranial pressure and soon entered a coma. More than 48 hours, the pillow was smashed and died.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.