(I) Treatment
1. Principles of emergency treatment for acute cerebral hemorrhage
①Prevent further bleeding; ②Lower intracranial pressure; ③Control cerebral edema; ④Maintain vital functions and prevent complications Specific measures are.
(1) Quiet bed rest: elevate the head of the bed and minimize moving.
(2) Ensure unobstructed airway: the initial 5 min of cerebral hemorrhage is crucial for life. As the patient’s tongue drops back, it is easy to obstruct the airway and cause asphyxia.
(3) Reasonable application of sedative drugs: sedative, antispasmodic and analgesic drugs should be applied to those who are agitated or epileptic.
(4) Regulation of blood pressure: for cerebral hemorrhage with high blood pressure, small doses of moderate antihypertensive agents can be used cautiously Oral antihypertensive drugs should be given to those with clear consciousness
(5) Less moving: If the patient has an attack in a small place, try to move to a spacious place as soon as possible. The principle is to try not to shake the head and keep the head in a horizontal position to avoid blocking the airway.
(6) Internal medicine treatment: the hematoma is small and there is no obvious increase in intracranial pressure. Basically, basic internal medicine treatment is the mainstay, and sometimes drugs to improve cerebral blood circulation can be added early.
(7) Surgical treatment: For patients with large hematoma and obvious displacement of midline structures, most of them should be operated in time. Sometimes, in order to save critically ill patients, emergency surgery is required. Thus, a better outcome can be achieved.
(8) Hemostatic drugs: commonly used phenolsulfonamide (hemostasis), aminobenzoic acid (antifibrinolytic aromatic acid), vitamin K, etc. The dosage of hemostatic drugs should not be too large, and there should not be too many types.
(9) strengthen care to keep the respiratory tract unobstructed: regular turning and back patting to prevent pneumonia and bed sores focus on dynamic observation of vital signs, including consciousness, pupils, blood pressure, pulse, respiration, measured once every half hour after stabilization can be measured once every 2 to 4 hours and carefully recorded
(10) Timely resuscitation: If consciousness becomes more impaired or agitated, both pupils are unequal in size, slow response to light, and blood pressure is elevated, it means brain herniation has occurred.
2. General treatment in the acute stage
(1) Keep the airway unobstructed: comatose patients should be placed in the lateral position, but not in the supine position, to prevent the tongue from falling back and blocking the airway. Turn over and pat the back regularly to facilitate the coughing out of sputum. lead to cerebral vasospasm and even oxygen toxicity
(2) Maintain nutrition and water-electrolyte balance: usually fasting is preferable during the first two days of the disease, and the daily infusion should be 1500-2000ml, and record the in and out volume. If there is high fever, vomiting, sweating, excessive diuresis, etc., increase as appropriate. Avoid the use of high-sugar fluids and give fat emulsion injection (fat milk), human albumin, amino acid or energy combination, etc., if necessary.
(3) Strengthen nursing care: Patients with cerebral hemorrhage have rapid onset, critical condition, and high mortality rate, so the care of the acute phase is crucial.
3. adjustment of blood pressure The principles of early antihypertensive treatment for patients with hypertensive cerebral hemorrhage are.
(1) Carefully grasp the indications for antihypertensive treatment It is generally considered that when the systolic blood pressure exceeds 24-26.66 kPa (180-200 mmHg), appropriate lowering of blood pressure can be considered to prevent further bleeding, but patients with excessive pulse pressure should be cautiously lowered
(2) Blood pressure should be controlled steadily so that the “peaks” and “troughs” of blood pressure in 24h are close to each other. This can avoid damage to the blood vessel wall from blood pressure fluctuations and prevent possible cerebral under-perfusion due to low blood pressure. Repeatedly, in large quantities or even in combination with a variety of strong antihypertensive drugs, such as converting enzyme inhibitors and other oral antihypertensive drugs or diuretics, but strong vasodilators should be used with caution or not. When the patient is completely insensitive to the antihypertensive response, attention should be paid to the increase in blood pressure due to intracranial hypertension.
(3) Do not lower the blood pressure too quickly It is more feasible to gradually lower the blood pressure to the above level or slightly higher over a period of time without the discomfort of cerebral ischemia Most believe that the blood pressure should be stabilized at about 20-21.33/12-13.33kPa (150-160/90-100mmHg) It is best to maintain it at a level slightly higher than the patient’s original blood pressure
(4) While using dehydrating and diuretic drugs for lowering cranial pressure and anti-cerebral edema treatment, the blood pressure, peripheral circulation and water and electrolyte balance must be closely monitored. However, the continuous decrease in blood pressure and the sudden decrease in blood volume and the disturbance of water electrolytes caused by the continuous use of large doses of this drug must be taken seriously.
(5) While applying antihypertensive drugs, the change in blood pressure should be observed. If the blood pressure is too low, the head of the bed should be lowered. If the blood pressure continues to be too low, appropriate antihypertensive drugs should be used to maintain the above level.
4. Control cerebral edema
After cerebral hemorrhage, cerebral edema gradually increases and often starts to appear within 6 hours and peaks within 3-4 days. Unless the patient is awake, the increase in intracranial pressure is not serious and there is no vomiting, oral medication can be used. In case of deep coma or early signs of brain herniation, strong dehydrating agents should be used. Usually, 2 to 3 types should be used alternately, such as 20% mannitol, furosemide (tachyphylaxis), glycerine preparations, and in case of cardiac or renal insufficiency, furosemide (tachyphylaxis) should be used first.
Dexamethasone has the strongest anti-cerebral edema effect among adrenocorticosteroids, especially for vasogenic cerebral edema. The dosage is usually 10-15mg in glucose solution or mannitol, and the dosage is reduced to discontinued within 1 to 2 weeks. In addition, the effect of hormones on reducing intracranial pressure is slow, and they cannot rapidly combat cerebral edema, so they are not recommended for routine use, especially for those with diabetes, hypertension, ulcer disease, and should be used with caution or forbidden because they may induce stress gastric bleeding.
5. Application of hemostatic drugs
Whether hemostatic drugs should be used in patients with cerebral hemorrhage is still a matter of opinion. Various hemostatic drugs can mainly stop capillary hemorrhage or leakage of blood from the brain parenchyma, and their effect on hemorrhage caused by arterial rupture is not certain.
For patients with atherosclerosis, the risk of ischemic cerebrovascular disease, myocardial infarction or renal artery thrombosis may increase, so some people oppose the use of hemostatic drugs. For patients with gastrointestinal bleeding, hemostatic drugs can be used, but the coagulation function should be checked frequently and short-term medication should be used under the supervision of relevant laboratory indicators. For patients with cerebral bleeding into the ventricles or subarachnoid space, appropriate hemostatic drugs can be considered to prevent rebleeding.
6. Artificial hibernation and hypothermia therapy
Artificial hibernation therapy can reduce the basal metabolic rate of the brain, reduce oxygen consumption and increase the tolerance of the brain to hypoxia, thus improving the state of cerebral hypoxia, reducing cerebral edema, lowering intracranial pressure, which has a protective effect on brain tissue and can also reduce or avoid rebleeding.
(1) Early hypothermia: try to give it within 6h of onset of the disease. The protective effect of cerebral hypothermia is poor beyond 7~8h.
(2) cooling methods: there are many cooling methods at present, it is necessary to set up advanced hypothermia room. If conditions are limited, the method of head ice cap + aorta ice + drugs can be used.
(3) the principle of gradual rewarming: first stop using drugs, then remove the ice, and finally remove the ice cap that can be completed within 8-12h; this short-term hypothermia rarely has complications, part of the emergence of myofibrillation and irritability can be given atracurium (carminative) 25mg or valium 10mg
7. Surgical treatment
With the development of microsurgery, stereotactic surgery and other techniques, the accuracy of surgery has been improved and the trauma to brain tissue has been greatly reduced. The indications for surgery for hypertensive cerebral hemorrhage have been broadened.
It is generally believed that the hematoma forms within 6 hours after the onset of hemorrhage, and the edema reaches its peak 8-24 hours after hemorrhage. Removing the hematoma before then may lead to better functional recovery. Early surgery can not only remove the hematoma in time to resolve the intracranial hypertension, but also reduce the damage to the brain tissue caused by blood decomposition, which is important to reduce the death and disability rates.
(1) Indications for surgery: There is no unified standard for surgical indications for the treatment of hypertensive cerebral hemorrhage. It is generally considered that the patient is not particularly old, has good function of important organs, has no serious complications such as deep coma, gastrointestinal bleeding, decortical ankylosis, double pupil narrowing and central hyperthermia, etc., and meets one of the following conditions: ① bleeding volume of 20 ml or more, ② hematoma in the thalamus or basal nucleus, ③ rupture into the ventricles, if ③If the cerebral water circulation is affected, ventricular puncture and drainage should be performed as soon as possible, and lumbar puncture should be performed once a day to release 10-20 ml of cerebrospinal fluid each time until the condition stabilizes. (2) The timing of surgery
(2) Timing of surgery: In the past, it was thought that patients with cerebral hemorrhage were in critical condition in the early stage and that surgery was dangerous and risked rebleeding. As research progresses, most scholars advocate early or ultra-early surgery, i.e., surgery within 6-8 hours of onset, before the development of edema in the brain tissue surrounding the hematoma. This can not only relieve the compression of the brain tissue by the hematoma, but also avoid the development of cerebral edema, and break the vicious cycle caused by the decomposition of blood cells and brain tissue edema after hemorrhage. For those who have hemorrhage for more than 20 days, whether to use puncture should be determined according to the specific situation.
(3) Surgical methods: commonly used surgical methods for hematoma removal include: ① neuroendoscopic treatment techniques; ② minimally invasive surgery for hypertensive cerebral hemorrhage; ③ bone flap or bone window craniotomy for hematoma removal; ④ CT-guided stereotactic aspiration treatment; ⑤ ventricular drainage hematoma lysis
8. Recovery treatment of cerebral hemorrhage
The purpose of recovery treatment is to promote the recovery of paralyzed limbs and speech impairment, improve brain function, reduce sequelae and prevent recurrence. The timing of recovery treatment is when the brain lesions are basically stable, cerebral edema and clinical symptoms of intracranial hypertension subside, and the damaged brain function gradually recovers. Another important therapeutic measure in the recovery period is rehabilitation, especially for patients with severe neurological deficits such as hemiplegia and aphasia, which should be started as early as possible and carried out in a systematic manner in order to achieve better results and significantly reduce disability.
(1) Prevention of rebleeding: recurrent cerebral hemorrhage is one of the main causes of death and disability among survivors of cerebrovascular disease. In China, Song Degen et al. reported that the interval of recurrent cerebral hemorrhage ranged from 3 months to 5 years, accounting for 19.5% (58/297) of cerebral hemorrhage in the same period. Recurrence
Regarding the causative factors of rebleeding, Passeros et al. showed that the risk factors for recurrent cerebrovascular disease were not significantly related to age, sex, hyperlipidemia, smoking, heavy alcohol consumption and diabetes mellitus, but rather to uncontrolled hypertension and vascular amyloidosis.
In China, Song Degen et al. concluded that hypertension is the most common cause of rebleeding, followed by emotional changes such as excitement, sadness, diabetes mellitus, and a history of TIA or ischemic cerebrovascular disease in the elderly, and rebleeding in hyperlipidemia is less common. Therefore, active control of hypertension, reasonable treatment of diabetes mellitus, and attention to self-regulation of emotions, regularity of life, moderate diet, and timely treatment of constipation are important aspects of preventing rebleeding. Regarding the regression of rehemorrhage, Song Degen et al. reported that 58 cases were treated with internal medicine, 29 cases improved and 29 cases died, accounting for 50% of the number of patients each.
(2) Drug treatment.
Calcium channel antagonists: after cerebral hemorrhage, cerebral tissue around hematoma ischemia and hypoxia, nerve cells in the lesion are in calcium overload, and calcium channel antagonists can reduce the overload state to prevent cell death, improve cerebral microcirculation, and increase cerebral blood flow supply. 3 times/d hypotension, cerebral edema, increased intracranial pressure, use with caution
② brain metabolism activator: can be used to promote neurometabolism drugs such as piracetam (brain regain Kang) cytophosphatidylcholine (cytophosphatidylcholine) brain protein hydrolysate (brain activator) γ-aminotyrosine pantothenic acid (coenzyme Q10) vitamin B family, vitamin E and vasodilator drugs can also be used to activate blood circulation, resolve blood stasis, and benefit qi and ligament and other formulas
(3) Diet control.
① should provide nutritious and easily digestible food to meet the body’s demand for protein, vitamins, inorganic salts and total caloric energy
(2) Drink more water and eat semi-liquid food because paralyzed patients often have the psychology of drinking as little water as possible for fear of urinating too much, which is detrimental to the patients.
③ Pay attention to the supply of fiber in the diet, so as to prevent constipation, avoid strong tea, alcohol, coffee and spicy food.
④Control salt and cholesterol intake and increase B vitamin-rich foods.
(4) Rehabilitation treatment.
①Passive exercise and massage: When the patient’s limbs have no muscle strength, passive exercise should be the mainstay. The movements should be gentle, gentle and rhythmically performed joint by joint to ensure the full range of motion of all joints. The passive exercise should pay special attention to the abduction and external rotation of the shoulder joint on the affected side to prevent painful contracture of the shoulder joint.
②Active exercise: After the patient has muscle strength, active exercise should be carried out in a timely manner.
Active movement in bed and sitting training: Some patients with cerebrovascular disease initially see themselves as the whole limb of paralysis rather than just one side of paralysis and feel completely powerless. The first way to overcome this feeling is to help patients learn to use the limb on the side of the bed to move the body and to make supine limb extension and flexion movements. Such as pulling a rope, practicing sit-ups, reaching in the supine position, lifting the leg so that the tightened muscles are pulled strongly to increase the range of motion
Bedside exercise: Patients should gradually learn to sit up at the bedside by curling up on their healthy side and then placing the healthy lower limb under the affected lower limb to lower the affected limb from the bedside and sit up with the support of the healthy upper limb. At this time, patients are using visual afferents and proprioceptive afferents from the healthy upper limb to fully learn and train sitting balance. After learning sitting balance, it is much easier to learn standing balance.
Standing exercise: after being able to exercise at the bedside, create the conditions to achieve self-reliance by holding a human crutch or leaning against the wall, and then leave the bed to move around indoors and outdoors
③Physical therapy and acupuncture treatment
④Medical sports therapy: The coordination of the body is produced by frequent and repeated training. When a limb is paralyzed, the coordination is lost. Each group of muscles will progress from simple to complex and through repeated physical exercise, the function of the limbs will gradually be coordinated.
9. Stroke unit treatment model of cerebrovascular disease
(1) What is a stroke unit: A stroke unit is a model of stroke treatment management that provides systematic medication, physical rehabilitation, language training, psychological rehabilitation and health education for stroke patients.
The characteristics of the stroke unit can be summarized from the above concepts as
(i) It is not a green channel for acute care, nor is it a full stroke management, but only a management of patients during their stay in hospital.
(ii) The stroke unit is not a therapy, but a ward management system that does not include new treatments.
(3) The new ward management system should be a multidisciplinary care system, i.e., a multidisciplinary collaboration.
(4) Patients should receive rehabilitation and health education in addition to medication, but a stroke unit is not the same as medication plus rehabilitation, it is a special type of integrated eare or organized care.
(5) The stroke unit reflects the humanistic care of the patient and the humanistic approach. It takes the patient’s functional prognosis and the satisfaction of the patient and the family as the important clinical objectives, unlike the treatment in the traditional ward, which only emphasizes the recovery of neurological function and improvement of imaging.
(2) Stroke units can be divided into four basic types as follows.
(1) Acute stroke unit: Patients in the acute phase are usually admitted within one week of onset.
(ii) rehabilitation stroke unit: patients admitted after 1 week of onset of stroke, as the condition is stable, more emphasis is placed on rehabilitation, and patients are hospitalized for several weeks or even months
③combined acute and rehabilitation stroke unit: also called comprehensive stroke unit, which combines the functions of acute and rehabilitation and treats patients in the acute phase, but hospitalization can be extended to several weeks or even months if needed.
mobile stroke unit: also called mobile stroke team In this model, there is no fixed ward, patients are admitted to different wards and a multidisciplinary team visits the ward and develops a medical plan, so there is no fixed care team. stroke team)
(3) All stroke patients should be treated in a stroke unit: Stroke units are a common form of stroke care and it is not difficult to set up a stroke unit.
The need for admission to a stroke unit (e.g. stroke unit, early intervention in rehabilitation, multidisciplinary team) is particularly emphasized in the recent Royal Society of Medicine guidelines (2000), the European Stroke Association guidelines (2000) and the American Stroke Association guidelines (2003).
The Beijing organized stroke care system BOCSS project, which was launched in 2002, will greatly contribute to the improvement of stroke care in China and to the international system.
(ii) Prognosis
The hematoma usually dissolves spontaneously after 1 week, and the clot is gradually absorbed. The cerebral edema and increased intracranial pressure gradually decrease, and the patient gradually becomes conscious.
1. Factors with poor prognosis
(1) Large hematoma, severe brain tissue destruction, and sustained intracranial pressure increase
(2) Significant impairment of consciousness
(3) Upper gastrointestinal bleeding
(4) Brain herniation formation
(5) Central hyperthermia
(6)Decortical tonicity
(7)senior patients over 70 years of age
(8)Complications of respiratory or urinary tract infection
(9)recurrent cerebral hemorrhage
(10) High or low blood pressure Cardiac insufficiency These patients can be life-threatening or left with severe limb paralysis or prolonged impairment of consciousness
2. Factors affecting the morbidity and mortality of patients with hypertensive atherosclerotic cerebral hemorrhage
(1) Generally older age and high mortality rate, therefore, the treatment of cerebral hemorrhage in the elderly should be taken with positive and cautious attitude
(2) High mortality rate in patients with underlying diseases and comorbidities, such as arteriosclerosis, diabetes mellitus, coronary heart disease, emphysema, etc., whose vital organs have poor reserve function, reduced stress and defense ability, and prone to multi-organ failure, high mortality rate, and concurrent infections during treatment and morbidity, electrolyte, acid-base imbalance, hypovolemic state and medical factors, etc., seriously affect the normal metabolism of major organs and reduce their functions.
(3) Infection is one of the main causes of multi-organ failure and death, so the rational application of antibiotics to control infection is the key to prevent and treat multi-organ failure.
(4) Combined upper gastrointestinal hemorrhage is an important sign of dangerous condition Combined upper gastrointestinal hemorrhage increases the death rate in patients with a history of gastric disease, especially if the hematoma has broken into the ventricle, which is probably the most dangerous factor leading to upper gastrointestinal hemorrhage
(5) Death in patients with cerebral hemorrhage is significantly correlated with the site of hemorrhage, the volume of hemorrhage, and the accumulation of blood in the ventricles. The greater the volume of hemorrhage, the more severe the compression of the surrounding brain tissue, the more pronounced the cerebral edema and the increase in intracranial pressure.
(6) A large amount of blood accumulation in the third and fourth ventricles can cause obstruction of the midbrain aqueduct, leading to acute obstructive hydrocephalus, aggravating cranial hypertension and cerebral edema, and blood cerebrospinal fluid can also directly stimulate the subthalamus, leading to neuroendocrine dysfunction, resulting in hyperthermia, upper gastrointestinal bleeding, cerebrocardiac syndrome, hyperglycemia, and other complications.
(7) Blood accumulation in the fourth ventricle can also cause dilatation of the fourth ventricle and direct compression of the brainstem, leading to brain herniation or respiratory arrest.
(8) The morbidity and mortality rate is significantly higher in cases where the hematoma breaks into the ventricle than in cases where the hematoma does not break into the ventricle. If the hematoma breaks into the ventricle and the blood clot blocks the cerebrospinal fluid pathway, hematoma removal and continuous drainage of the ventricle should be performed, which can greatly reduce the morbidity and mortality rate.
(9) The immediate cause of death in early cerebral hemorrhage is mainly cerebral herniation. Therefore, rapid and effective relief of cerebral compression and acute cranial hypertension is the key to successful treatment. When the occupying effect is aggravated by hemorrhage and/or edema, resulting in deterioration of neurological function, aggressive therapeutic measures should be used.
(10) Comprehensive therapeutic measures: In the treatment of patients with cerebral hemorrhage, in order to reduce the morbidity and mortality rate, in addition to active treatment of the original disease, comprehensive treatment should be provided to prevent and treat upper gastrointestinal bleeding, acute renal failure, secondary infections and other complications.