Cerebral hemorrhage is a non-traumatic bleeding in the brain parenchyma. The incidence rate is 60-80/100,000 population/year, accounting for about 30% of acute cerebrovascular diseases in China. The death rate in the acute phase is about 30% to 40%, which is the highest among acute cerebrovascular diseases. Among brain hemorrhage, hemorrhage in the cerebral hemisphere accounts for about 80%, and hemorrhage in the brainstem and cerebellum accounts for about 20%. CT scan of the brain is the most effective and rapid method to diagnose cerebral hemorrhage. The treatment of cerebral hemorrhage is to promptly remove the hematoma, actively reduce the intracranial pressure, and protect the brain tissue around the hematoma if indicated.
I. Diagnosis
(A) General diagnosis
1. Clinical characteristics
(1)Acute onset under dynamic;
(2) Sudden onset of focal neurological deficits, often accompanied by headache and vomiting, may be accompanied by increased blood pressure, impaired consciousness and meningeal irritation signs.
2.Auxiliary examination
(1) Blood tests: there may be increased white blood cells and elevated blood sugar, etc;
(2) Imaging examinations.
(1) CT scan of the head: it is a safe and effective method to diagnose cerebral hemorrhage, which can accurately and clearly show the site of cerebral hemorrhage, the amount of hemorrhage, the occupying effect, whether it breaks into the ventricle or subarachnoid space and the damage of surrounding brain tissue. CT scan of cerebral hemorrhage shows hematoma foci as high-density shadow with clear boundary and CT value of 75-80 Hu; after the hematoma is absorbed, it shows low-density shadow.
② Cephalometric MRI examination: After cerebral hemorrhage, with the extension of time, the oxygenated hemoglobin (HbO2) in intact red blood cells gradually transformed into deoxygenated hemoglobin (DHb) and methemoglobin (MHb), and after the fragmentation of red blood cells, methemoglobin precipitated in a free state and finally became iron-containing heme. The above evolutionary process progresses from the periphery to the center of the hematoma, so the MRI manifestation of the hematoma varies at different times after hemorrhage. CT is superior to MRI in the diagnosis of acute cerebral hemorrhage, but MRI can show the evolution of the hematoma more accurately and can be useful in the exploration of the etiology of certain patients with cerebral hemorrhage, such as better identification of aneurysmal stroke and detection of AVM and aneurysm.
③ Cerebral angiography (DSA): Cerebral angiography should be performed in young and middle-aged people with non-hypertensive cerebral hemorrhage, or when vascular abnormalities are suspected on CT and MRI examinations. Cerebral angiography can clearly show the abnormal blood vessels and show the ruptured vessels and sites of contrast leakage.
(3) Lumbar puncture: When cerebral hemorrhage breaks into the ventricle or subarachnoid space, lumbar puncture can reveal bloody cerebrospinal fluid. In the absence of conditions or CT scan, lumbar puncture can be performed to assist in the diagnosis of cerebral hemorrhage, but the positive rate is only about 60%. For massive cerebral hemorrhage or early cerebral herniation, lumbar puncture should be performed with caution to avoid inducing cerebral herniation.
(4) Estimation of blood volume: The clinic can use the easy-to-use Tada’s formula to estimate the bleeding volume based on CT images. The method is as follows.
Bleeding volume = 0.5 × maximum area long axis (cm) × maximum area short axis (cm) × number of levels, V = 1/2L × W × S.
(B) Key points of clinical diagnosis of cerebral hemorrhage in various areas
1. Shell nucleus hemorrhage: It is the most common cerebral hemorrhage, accounting for about 50% to 60%, and the hemorrhage often spreads to the internal capsule.
(1) Contralateral limb hemiparesis, dominant hemisphere hemorrhage often appears aphasia.
(2) Sensory impairment of the contralateral limb, mainly hyperalgesia and hypothermia.
(3) Contralateral hemianopia.
(4) Gaze palsy, with persistent bilateral gaze to the side of the hemorrhage.
(5) Disuse, body image impairment, memory and calculation impairment, and consciousness impairment may also occur.
2.Thalamic hemorrhage: about 20% of the cases.
(1) Thalamic sensory disorder: contralateral hemianesthesia, sensory hypersensitivity or spontaneous pain.
(2) Motor disorders: hemorrhage invading the internal capsule can appear contralateral limb paralysis, mostly lower limbs than upper limbs.
(3) Thalamic aphasia: slow and unclear speech, repetitive speech, difficulty in articulation, poor repetition, and normal reading aloud.
(4) Thalamic dementia: memory loss, decreased calculation, emotional disturbance, and personality changes.
(5) Oculomotor disorders: paralysis of upward gaze of the eye, often gazing inward and downward.
3, brainstem hemorrhage: about 10%, the majority of cerebral bridge hemorrhage, occasionally seen in the midbrain hemorrhage, medulla oblongata hemorrhage is extremely rare.
(1) Midbrain hemorrhage: sudden onset of diplopia, eyelid ptosis; pupil dilation on one or both sides, different axes of the eye, horizontal or vertical nystagmus, ataxia of the ipsilateral limb, and also Weber or Benedikt syndrome; severe cases soon appear impaired consciousness, de-brain tonicity.
(2) Cerebral bridge hemorrhage: sudden headache, vomiting, vertigo, diplopia, different axes of the eye, crossed paresis or hemiparesis, and quadriplegia. When the hemorrhage is large, the patient quickly enters into consciousness disorder, pinpoint pupils, denervation tonicity, respiratory disturbance, and mostly dies rapidly, and may be accompanied by high fever, profuse sweating, stress ulcers, etc.; when the hemorrhage is small, it may manifest as some typical syndromes, such as Foville, Millard-Gubler and atresia syndromes, etc.
(3) Medullary hemorrhage: sudden impairment of consciousness, drop in blood pressure, irregular respiratory rhythm, cardiac rhythm disturbance, followed by death; milder cases may manifest as atypical Wallenberg syndrome.
4, cerebellar hemorrhage: about 10%.
(1) Sudden onset of vertigo, vomiting, posterior head pain, without hemiparesis.
(2) There are nystagmus, unstable standing and walking, limb ataxia, decreased muscle tone and cervical ankylosis.
(3) CT scan of the head shows high-density shadow of cerebellar hemispheres or earthworms and compression of the four ventricles and brainstem.
5.Lobar hemorrhage: about 5% to 10%.
(1) Frontal lobe hemorrhage: forehead pain, vomiting, epileptic seizures are more common; contralateral hemiparesis, common hemianopia, mental disorder; motor aphasia may occur in the case of dominant hemisphere hemorrhage.
(2) Parietal hemorrhage: hemiparesis is milder, while hemianopsia is significant; contralateral lower quadrant blindness; mixed aphasia may occur in case of dominant hemisphere hemorrhage.
(3) Temporal lobe hemorrhage: manifests as contralateral central facial and tongue paresis and upper limb dominant paresis; contralateral upper quadrant blindness; sensory aphasia or mixed aphasia may occur in case of dominant hemisphere hemorrhage; temporal lobe epilepsy, phantom smell and phantom vision may be present.
(4) Occipital hemorrhage: contralateral isotropic hemianopia with macular avoidance, transient blackness and visual deformation; no limb paralysis.
6. Ventricular hemorrhage: about 3% to 5%.
(1) Sudden headache, vomiting, rapidly enter coma or coma gradually deepen.
(2) Bilateral pupil narrowing like a pinpoint, increased muscle tone of limbs, positive pathological reflexes, early appearance of decerebrate tonicity, positive meningeal stimulation sign.
(3) Signs and symptoms of subthalamic damage are often present, such as upper gastrointestinal bleeding, central hyperthermia, profuse sweating, stress ulcers, acute pulmonary edema, increased blood glucose, and uremia.
(4) Cerebrospinal fluid pressure is elevated and bloody.
(5) Mild cases only show headache, vomiting, positive meningeal irritation signs, and no restricted neurological signs. It is easily misdiagnosed clinically as subarachnoid hemorrhage, and a cranial CT scan is required to confirm the diagnosis.
(C) Etiology of cerebral hemorrhage
The etiology of cerebral hemorrhage is diverse and should be clarified as much as possible to facilitate treatment. The following are the common etiologies and diagnostic clues.
1. Hypertensive cerebral hemorrhage
(1)It is common in people over 50 years old.
(2) There is a history of hypertension.
(3) The common sites of hemorrhage are the nucleus accumbens, thalamus, cerebellum and cerebral bridge.
(4) There is no evidence of cerebral hemorrhage such as trauma and amyloid angiopathy.
2.Hemorrhage from cerebrovascular malformation
(1)It is common in young people.
(2)The common site of hemorrhage is the cerebral lobe.
(3) Imaging can find abnormal images of blood vessels.
(4) Confirmation of diagnosis needs to be based on cerebral angiography.
3.Brain amyloid angiopathy
(1) It is mostly seen in elderly patients or patients with familial cerebral hemorrhage.
(2) Mostly without a history of hypertension.
(3) The common site of hemorrhage is the cerebral lobe, and multiple cases are more helpful for diagnosis.
(4) There is often a history of recurrent cerebral hemorrhage.
(5) Pathological histological examination is needed to determine the diagnosis.
4.Brain hemorrhage due to thrombolytic therapy
(1)Thrombolytic drugs have been applied recently.
(2) The hemorrhage is mostly located in the lobes of the brain or near the original cerebral infarction lesion.
5.Cerebral hemorrhage caused by anticoagulation therapy
(1) Recently treated with anticoagulants.
(2) Lobar hemorrhage is common.
(3) There is mostly a tendency to continue bleeding.
6.Tumor stroke
(1) Focal neurological symptoms are present before the cerebral hemorrhage.
(2) The hemorrhage is often located in an atypical site of hypertensive cerebral hemorrhage.
(3) Significant edema around the hematoma appears early on imaging.
II. Treatment
(A) Internal treatment of acute cerebral hemorrhage
1.General treatment
(1) Bed rest: Generally, bed rest should be taken for 2 to 4 weeks to avoid emotional excitement and elevated blood pressure.
(2) Keep the airway unobstructed: comatose patients should tilt their heads to the side to facilitate the flow of oral secretions and vomit, and prevent the backward fall of the tongue from obstructing the airway, suck out the oral secretions and vomit at any time, and preferably perform tracheotomy in time.
(3) Oxygen: Patients with impaired consciousness, decreased oxygen saturation or hypoxia (PO250mmHg) should be given oxygen.
(4) Nasal feeding: Those who are comatose or have difficulty swallowing should be given nasal feeding on the second to third day of illness.
(5) Symptomatic treatment: Patients who are excessively agitated can be sedated in appropriate amounts; constipated patients can use laxatives.
(6) Prevention of infection: strengthen oral care, timely aspiration, and keep the respiratory tract unobstructed; bladder flushing should be done when catheterization is in place, and antimicrobial agents can be used to prevent infection in comatose patients as appropriate.
(7) Observe the condition: pay close attention to the patient’s consciousness, pupil size, blood pressure, respiration and other changes, and perform intracranial pressure monitoring in comatose patients when available.
2. Regulation of blood pressure
The control of blood pressure in patients with cerebral hemorrhage does not have a certain standard, and should depend on the patient’s age, previous hypertension, the presence of increased intracranial pressure, the cause of bleeding, and the time of onset. The following principles can be generally followed.
(1) Patients with cerebral hemorrhage should not be in a hurry to lower blood pressure because the increase in blood pressure after cerebral hemorrhage is a reflexive self-regulation of the increased intracranial pressure, and the decision to lower blood pressure treatment should be made according to the blood pressure situation after the intracranial pressure has been lowered first.
(2) When the blood pressure is ≥200/110mmHg, the cranial pressure can be lowered at the same time with careful and smooth blood pressure lowering treatment, so that the blood pressure is maintained at a level slightly higher than the pre-onset level or around 180/105mmHg; if the systolic blood pressure is 170-200mmHg or diastolic blood pressure is 100-110mmHg, there is no need to use antihypertensive drugs for the time being, first dehydrate and lower the cranial pressure, and closely observe the blood pressure situation, and then if necessary Use antihypertensive drugs if necessary. The blood pressure should not be reduced too much, otherwise it may cause cerebral hypoperfusion.