Features
Features:

Product Tour >

Edraw AI >

Paid Plans:

Individuals >

Business >

Eduaction >
Resources
Blog

History

How-tos & Tips

Discovery

Biography

Business Analysis

Examples

AI concept Map

Free AI Mind Map Generator

Onenote Mind Map

Bcg Matrix Examples

Nike Marketing Strategy

Unilever SWOT Analysis

Make Mind Maps in Google Docs

Guide

FAQs

What's New

Resource Center
Templates
All Templates

Brain Storming Templates

Strategy and Planning Templates

Project Management Templates

Product Management Templates

Human Resources Templates

Agile Workflow Templates

Marketing Templates

Education Templates

Fun and Games Templates

User Gallery
Download
Pricing
Enterprise

MindMap Gallery 8.2. Cerebral hemorrhage

8.2. Cerebral hemorrhage

Neurology - Detailed explanation of the knowledge framework of cerebrovascular disease and intracerebral hemorrhage. Including etiology, pathogenesis, pathology, clinical manifestations, treatment, prognosis, etc.

Edited at 2023-11-12 17:29:34

PlotWizard

Recent works View more works>>

8.2. Cerebral hemorrhage

PlotWizard

Recent works View more works>>

Recommended to you
Outline

intracerebral hemorrhage ICH

non-traumatic intraparenchymal hemorrhage

Cause

The most common cause is hypertension combined with arteriosclerosis. Other causes include arteriovenous malformations, cerebral amyloid vasculopathy, hematological diseases (such as leukemia, aplastic anemia, thrombocytopenic purpura, hemophilia, polycythemia, and sickle cell disease, etc.), anticoagulation or thrombolytic therapy, etc.

Pathogenesis

It is mainly caused by the rupture of chronic lesions in the small arteries in the brain under the action of long-term hypertension.

Intracranial arteries are characterized by fewer muscle cells in the middle layer, less outer connective tissue, and loss of the external elastic lamina. Long-term hypertension can cause hyaline degeneration, fibrous cord-like necrosis, and even microaneurysms or dissecting aneurysms in small cerebral arteries. On this basis, a sudden increase in blood pressure can easily lead to blood vessel rupture and bleeding.

Deep perforating arteries such as the lenticulostriate artery and the paramedian artery originate from the arteries at the base of the brain at right angles. They bear the impact of high-pressure blood flow and can easily cause blood vessel rupture and bleeding, so they are also called bleeding arteries.

pathology

cerebral hemorrhage

Hematoma compression and destruction

Brain edema

Inflammation

apoptosis

Perihematoma ischemia

clinical manifestations

(1) General performance

➢ Commonly seen in patients over 50 years old

➢ Slightly more men than women

➢ The incidence rate is higher in cold seasons

➢ Most have a history of hypertension

➢ It often occurs suddenly during emotional excitement or activity, and the condition often reaches its peak within minutes to hours after onset.

A small number of ICH can also occur in a quiet state. Prodromal symptoms are generally not obvious.

Most patients with ICH have significantly elevated blood pressure after onset. Due to increased intracranial pressure, headache, vomiting and varying degrees of consciousness disorders, such as drowsiness or coma, are common.

(2) Localized localization performance depends on the bleeding site and amount of bleeding

1. Bleeding in the basal ganglia

(1) Putamen hemorrhage: the most common

It is caused by the rupture of the lenticulostriate artery, especially its lateral branch, and can be divided into localized type (the hematoma is limited to the putamen) and extended type. Hemiparesis, sensory loss and homonymous hemianopia on the contralateral side of the lesion are common. Inability to gaze in the same direction to the contralateral side of the lesion may also occur. Aphasia may occur if the dominant hemisphere is involved.

(2) Thalamus hemorrhage:

Contralateral hemiplegia and hemi-sensory impairment are often present, and sensory impairment is usually more severe than motor impairment. Both deep and superficial senses are affected, but deep sensory impairment is more obvious. There may be characteristic eye signs, such as inability to look upward or staring at the tip of the nose, eyeball deviation or dissociative strabismus, eyeball convergence disorder, and unresponsive small pupils.

(3) Bleeding from the head of the caudate nucleus:

Headache, vomiting, neck stiffness, and mental symptoms are common. Symptoms of neurological deficit are rare, so the clinical symptoms are similar to subarachnoid hemorrhage.

2. Lobar hemorrhage

Bleeding is most common in the parietal lobe, followed by the temporal lobe, occipital lobe, and frontal lobe. There are also multiple cases of cerebral lobe hemorrhage.

Frontal lobe hemorrhage may cause hemiplegia, urinary and defecation difficulties, Broca's aphasia, groping and strong grip reflexes, etc.

Temporal lobe hemorrhage may cause Wernicke's aphasia, psychiatric symptoms, contralateral upper quadrant blindness, and epilepsy

Occipital lobe hemorrhage may cause visual field defects

Parietal lobe hemorrhage may cause hemiplegia, hemiparesis, and contralateral inferior quadrant blindness, and involvement of the non-dominant hemisphere may cause conformational disorders.

3. Brain stem hemorrhage

(1) Pontine hemorrhage:

➢Massive bleeding (hematoma >5ml)

The patient immediately developed coma, bilateral pinpoint pupils, vomiting of coffee-like gastric contents, central hyperthermia, central respiratory disturbance, floating eyeballs, quadriplegia, and decerebrate tonic seizures.

➢Small bleeding may cause unconsciousness

Manifested as crossed paralysis and ataxic hemiplegia, paralysis of both eyes staring to the side of the lesion or internuclear ophthalmoplegia

(2) Midcerebral hemorrhage:

➢Mild symptoms include unilateral or bilateral oculomotor nerve insufficiency paralysis, eyeball asymmetry, ipsilateral limb ataxia, and Weber or Benedikt syndrome.

➢Severe symptoms include deep coma, flaccid paralysis of the limbs, and rapid death.

(3) Medulla bulbar hemorrhage:

Even more rarely, the clinical manifestations are sudden disturbance of consciousness, affecting vital signs, such as changes in breathing, heart rate, and blood pressure, and then death. Mild patients may present with atypical Wallenberg syndrome

4. Cerebellar hemorrhage

Headache, vomiting, obvious dizziness and ataxia are common. The onset is sudden and may be accompanied by occipital pain.

Those with a small amount of bleeding mainly show symptoms of cerebellar damage, such as ataxia, nystagmus, and cerebellar speech on the affected side, and most of them do not suffer from paralysis.

For those with a large amount of bleeding, especially in the cerebellar vermis, the condition progresses rapidly, with signs of coma and brainstem compression appearing at the onset or within 12 to 24 hours after the illness, bilateral pupils shrinking to a pinpoint shape, irregular breathing, etc.

The fulminant type often causes sudden coma and rapid death within a few hours.

5. Intraventricular hemorrhage

primary intraventricular hemorrhage

Mostly caused by rupture and bleeding of choroid plexus vessels or subependymal artery

secondary intraventricular hemorrhage

Refers to cerebral parenchymal hemorrhage breaking into the ventricles

Headaches and vomiting are common, and in severe cases, disorders of consciousness may occur, such as deep coma, meningeal irritation, pinpoint pupils, eyeball separation, strabismus or floating, flaccid limb paralysis and decerebrate tonic attacks, high fever, irregular breathing, and unstable pulse and blood pressure. and other symptoms. Clinically, it is easy to be misdiagnosed as subarachnoid hemorrhage.

Auxiliary inspection

(1) CT examination

Brain CT scan is the preferred method for diagnosing ICH

The lesions are mostly round or oval uniform high-density areas with clear boundaries (CT characteristics of cerebral hemorrhage).

Dynamic CT examination can also evaluate the progression of bleeding.

(2) MRI and MRA examination

MRI is better than CT scan in detecting bleeding lesions in the brainstem and cerebellum and monitoring the evolution of cerebral hemorrhage, but it is inferior to CT in diagnosing acute cerebral hemorrhage.

(3) Cerebrospinal fluid examination

Patients with cerebral hemorrhage generally do not need to undergo lumbar puncture to avoid triggering brain herniation.

To rule out intracranial infection and subarachnoid hemorrhage, proceed with caution.

(4) DSA

Generally, DSA examination is not required unless vascular malformation, vasculitis or moyamoya disease is suspected and surgery or vascular interventional treatment is required.

DSA can clearly show abnormal blood vessels and ruptured blood vessels and locations of contrast medium leakage.

(5) Other inspections

Including blood routine, blood biochemistry, coagulation function, electrocardiogram and chest X-ray examination.

(1) Diagnosis

➢ Middle-aged and elderly patients

Age characteristics

➢ Sudden onset of illness during activities or when emotional

Onset characteristics

➢ Rapid onset of symptoms of focal neurological deficits

Clinical manifestations of neurological deficits

➢ If accompanied by symptoms of intracranial hypertension such as headache and vomiting, the possibility of cerebral hemorrhage should be considered

accompanying clinical manifestations

➢ Combined with head CT examination, the diagnosis can be confirmed quickly.

Auxiliary inspection

(2) Differential diagnosis

1. First, it should be distinguished from other types of cerebrovascular diseases such as acute cerebral infarction (P201) and subarachnoid hemorrhage (P218).

2. For those who become comatose suddenly and rapidly without obvious local signs, attention should be paid to systemic diseases that cause coma, such as poisoning (alcohol poisoning, sedative-hypnotic drug poisoning, carbon monoxide poisoning) and metabolic diseases (hypoglycemia, hepatic encephalopathy) , pulmonary encephalopathy and uremia, etc.) identification.

3. Patients with a history of head trauma should be distinguished from traumatic intracranial hematoma

treat

Treatment principles

Stay in bed quietly, dehydrate and lower intracranial pressure, adjust blood pressure, prevent and treat continued bleeding, and strengthen care to prevent and treat complications to save lives, reduce mortality, disability rates and recurrence.

The most important treatment is to reduce intracranial pressure and reduce cerebral edema

(1) Medical treatment

1. General processing

➢ Generally, you should rest in bed for 2 to 4 weeks, keep quiet, and avoid emotional agitation and elevated blood pressure.

➢ People with impaired consciousness and gastrointestinal bleeding should fast for 24 to 48 hours and empty their stomach contents if necessary.

➢ Pay attention to water and electrolyte balance, prevent aspiration pneumonia and actively control infection in the early stage.

➢ For patients with obvious headaches and excessive irritability, appropriate sedatives and analgesics may be given as appropriate. ➢ People with constipation can choose laxatives.

2. Reduce intracranial pressure

Cerebral edema can increase intracranial pressure and cause cerebral herniation, which is the main factor affecting mortality and functional recovery after cerebral hemorrhage.

Actively controlling cerebral edema and reducing intracranial pressure (ICP) are important steps in the treatment of acute cerebral hemorrhage.

3. Adjust blood pressure

4. Hemostatic treatment

5. Mild hypothermia treatment

6. Other treatments

(2) Surgical treatment

Surgical treatment

Purpose

1. Remove hematoma as soon as possible

2. Reduce intracranial pressure

3. Save lives

Indications

1. Moderate or larger amount of bleeding in the basal ganglia area (bleeding in the putamen ≥30ml, bleeding in the thalamus ≥15ml

2. Cerebellar hemorrhage ≥10ml or diameter ≥3cm, or combined with obvious hydrocephalus

3. Severe intraventricular hemorrhage (ventricular cast)

technique

1. Decompressive craniectomy

2. Small bone window craniotomy for hematoma evacuation

3. Drilling and aspiration of hematoma

4. Ventriculocentesis and drainage

(3) Rehabilitation treatment

prognosis

The overall prognosis is poor. Cerebral edema, increased intracranial pressure, and brain herniation are the main causes of death.