www.mingyihui.net Intracerebral Hemorrhage Treatment Guide (Introduction) (Part 3)

Guide to Seeking Medical Care for Cerebral Hemorrhage (Introduction Section) (3) Western Medicine Treatment Methods http://www.mingyihui.net/article_397.html

Drug Treatment

1. Principles of Emergency Treatment for Acute Cerebral Hemorrhage:

① Prevent further bleeding; ② Reduce intracranial pressure; ③ Control cerebral edema; ④ Maintain vital functions and prevent complications. Specific measures include:

(1) Rest in bed with the head of the bed elevated, minimizing movement. Generally, bed rest is recommended for about 3-4 weeks.

(2) Ensure airway patency: In the first 5 minutes after cerebral hemorrhage, life can be critically dependent on this. As patients are prone to asphyxiation due to posterior displacement of the tongue root blocking the airway, ensure the airway remains clear: loosen collars, remove dentures, place the patient in a lateral position with the head tilted back to facilitate the flow of oral secretions and promptly clear vomit from the mouth. If asphyxiation occurs, immediately clean the mouth and perform artificial respiration.

(3) Use sedatives appropriately: For agitated or epileptic patients, use sedatives, antispasmodics, and analgesics.

(4) Adjust blood pressure: For patients with high blood pressure, treatment options include small doses of Reserpine or a deep intramuscular injection of 10ml of 25% Magnesium Sulfate; conscious patients may be given oral antihypertensive drugs.

(5) Minimize moving the patient: If the patient becomes ill in a confined space, quickly move them to a more spacious area. The principle is to avoid shaking the head and maintain a horizontal position to prevent respiratory obstruction.

(6) Internal medicine treatment: If the hematoma is small with no significant increase in intracranial pressure, mainly internal medicine treatments are used. Early improvements in cerebral blood circulation may sometimes be added, often using traditional Chinese medicine preparations that promote blood circulation and remove blood stasis. Patients with accompanying cerebral edema and increased intracranial pressure require active and reasonable dehydration therapy.

(7) Surgical treatment: For large hematomas with obvious midline shift, timely surgery is generally required. Sometimes emergency surgery is needed for critically ill patients. Some scholars believe that hematoma plays an initiating and critical role in pathological damage, causing ischemic edema volume several times larger than the hematoma itself. Therefore, early surgery within 6 hours of onset can significantly reduce secondary damage, improve rescue success rates, and lower disability rates for better outcomes.

(8) Hemostatic drugs: Commonly used drugs include Etamsylate (Hemoclot), Aminomethylbenzoic Acid (Antifibrinolytic Fumaric Acid), Vitamin K, etc. Dosages should not be excessive, and the number of drug types should be limited.

(9) Strengthened nursing care, maintaining airway patency: Regularly turn the patient, tap their back, and prevent pneumonia and bedsores. Dynamically observe vital signs, including consciousness, pupils, blood pressure, pulse, and breathing every half hour, then stabilize to 2-4 hours, and meticulously record observations.

(10) Timely rescue: If consciousness deteriorates or the patient becomes restless with unequal pupil sizes, delayed light reflexes, slow pulse, and elevated blood pressure, it indicates a brain hernia has occurred and immediate rescue is necessary.

2. General acute phase treatment

(1) Keep the airway open: Comatose patients should be placed in a lateral position, avoiding supine positions to prevent posterior displacement of the tongue blocking the airway. Turn the patient regularly and tap their back to help cough up phlegm. Frequently suction secretions and use aerosol inhalation to humidify phlegm. Perform tracheotomy promptly if there are signs of airway obstruction to prevent oxygen deprivation which could worsen cerebral edema. Oxygen mixed with 5% carbon dioxide can be administered intermittently, avoiding prolonged pure oxygen inhalation which could lead to cerebral vasospasm or even oxygen poisoning.

(2) Maintain nutrition and electrolyte balance: It's typically best to withhold food for the first 1-2 days, with daily fluid intake ideally between 1500-2000ml, while recording input and output. When using large doses of dehydrating agents, pay attention to potassium supplementation. Additionally, prevent and correct acidosis, non-ketotic diabetes, and hyperosmolar coma. Insert a nasogastric tube for comatose or non-eating patients on the third day to ensure nutritional supply via liquid feeding. Appropriately limit fluid intake, generally not exceeding 2500ml per day, increasing as needed with fever, vomiting, excessive sweating, or overuse of diuretics. Avoid high-sugar fluids; fat emulsion injections, human serum albumin, amino acids, or energy complexes may be necessary.

(3) Strengthen nursing care: Acute cerebral hemorrhage has sudden onset, severe condition, and high mortality rate. Therefore, acute phase nursing is crucial. ① Closely monitor conditions, including consciousness, pupil changes, vomiting status, and monitoring blood pressure and temperature changes. ② Prevent complications: Prevention of complications is the main factor affecting acute cerebrovascular disease treatment and prognosis. Preventing urinary tract infections and decubitus ulcers is a nursing focus.

3. Adjusting Blood Pressure

The early antihypertensive treatment principle for hypertensive cerebral hemorrhage patients is:

(1) Carefully determine antihypertensive treatment criteria; generally, when systolic blood pressure exceeds 24～26.66kPa (180～200mmHg), consider appropriately lowering blood pressure to prevent further bleeding, but exercise caution with large pulse pressures.

(2) Control blood pressure steadily, making the "peak" and "trough" of 24-hour blood pressure close to each other. This prevents vascular wall damage from blood pressure fluctuations and avoids insufficient cerebral perfusion from excessively low blood pressure. Antihypertensive treatment should not overly pursue rapid results or repeatedly use large amounts of various potent antihypertensive drugs. Commonly use Reserpine (Rauwolfia) 0.5～1mg intramuscular injection, 10mg of 25% Magnesium Sulfate deep intramuscular injection, repeatable every 6～12h. Oral conversion enzyme inhibitors or diuretics can also be used, but strongly vasodilatory drugs should be cautiously or not used at all. If the patient is completely insensitive to antihypertensive responses, consider increased intracranial pressure-induced hypertension.

(3) Do not decrease blood pressure too rapidly; a feasible method is gradually reducing blood pressure over time to the above level or slightly higher without discomfort symptoms indicative of cerebral ischemia. Most recommend stabilizing blood pressure around 20～21.33/12～13.33kPa (150～160/90～100mmHg), preferably maintaining it slightly higher than the patient’s original blood pressure.

(4) While using dehydration and diuretic drugs for intracranial pressure reduction and anti-cerebral edema treatment, closely monitor blood pressure, peripheral circulation, and water-electrolyte balance. Especially with Furosemide (Lasix), continuous large doses causing sustained blood pressure drop, sudden reduction in blood volume, and water-electrolyte imbalance must be taken seriously.

(5) While using antihypertensive drugs, observe changes in blood pressure. If blood pressure is too high, elevate the head of the bed by approximately 30～45 degrees. When blood pressure approaches normal, lower the head of the bed. If blood pressure remains persistently low, appropriately use pressor drugs to maintain the above level.

4. Controlling Brain Edema

Reducing intracranial pressure is an important step in preventing the formation of brain hernias. After cerebral hemorrhage, brain edema gradually worsens, often starting within 6 hours, reaching its peak in 3～4 days, and gradually subsiding after half a month. The result of brain edema is increased intracranial pressure, potentially leading to brain hernias. Therefore, controlling brain edema and intracranial hypertension is key to reducing mortality rates. Timely active measures should be taken to control brain edema. Dehydration agents are generally administered intravenously or intramuscularly unless the patient is conscious, intracranial pressure is not severely increased, and there is no vomiting, in which case oral medications may be selected. When intravenous or oral administration is difficult, rectal instillation can be considered, such as 20% glycerin or 30% mannitol. In cases of severe dehydration with intracranial hypertension, 40～60ml of mannitol can be injected into the carotid artery to achieve brain tissue dehydration with minimal systemic impact. Consideration must be given to the degree of intracranial pressure elevation and overall conditions like heart and kidney function when selecting dehydration agents and dosages. In cases of deep coma or early signs of brain herniation, strong dehydration agents are necessary. Usually, 2～3 kinds should be alternately used, such as 20% mannitol, furosemide (lasix), and glycerol preparations. For patients with heart or kidney dysfunction, furosemide (lasix) is often used first. Colloidal solutions like 20% or 25% human serum albumin can prevent reduced blood volume and avoid hypotension.

During the acute phase, corticosteroids help reduce brain edema. Dexamethasone has the strongest anti-brain edema effect, particularly for vasogenic brain edema. A common dose is 10～15mg added to glucose solution or mannitol, administered intravenously over 1～2 weeks before tapering off. Since corticosteroids have a relatively slow effect and patients with brain hemorrhage are prone to gastrointestinal bleeding and pulmonary infections, they may exacerbate or mask the condition. Given the slow reduction in intracranial pressure and inability to quickly counteract brain edema, routine use is not recommended, especially for patients with diabetes, hypertension, or ulcers who should use cautiously or avoid them. Stress-induced gastric bleeding may occur easily, so concurrent use of gastric mucosal protective drugs is recommended.

5. Application of Hemostatic Drugs

There is still disagreement on whether hemostatic drugs should be used in cerebral hemorrhage patients. Various hemostatic drugs primarily stop bleeding or seepage from capillaries in brain tissue, but their effectiveness for arterial rupture-induced bleeding is uncertain.

Blindly applying hemostatic drugs might increase the risk of ischemic cerebrovascular disease, myocardial infarction, or renal artery thrombosis in patients with arteriosclerosis. Thus, some oppose the use of hemostatic drugs, recommending them only for those with gastrointestinal bleeding under regular coagulation function checks and short-term use guided by laboratory tests. For patients whose cerebral hemorrhage extends into the ventricles or subarachnoid space, appropriate hemostatic drugs can be considered to prevent rebleeding.

6. Artificial Hibernation Cooling Therapy

Artificial hibernation cooling therapy reduces the basic metabolic rate of the brain, decreases oxygen consumption, increases tolerance to hypoxia, thereby improving brain hypoxia, reducing brain edema, lowering intracranial pressure, and protecting brain tissue. It also helps reduce or avoid rebleeding.

(1) Early cooling: Ideally applied within 6 hours of onset, beyond 7～8 hours brain protection effects are poorer. Cooling should not exceed 48 hours, extendable if high fever complicates.

(2) Cooling methods: Many current cooling methods exist, advanced low-temperature rooms are useful. With limited conditions, ice caps on the head + ice packs on major arteries + medication can be used.

(3) Gradual rewarming principle: Stop medication first, then remove ice packs, finally the ice cap, completing within 8～12 hours; short-term low temperatures rarely cause complications, muscle tremors and agitation can be treated with Atracurium (Cisatracurium) 25mg or Diazepam 10mg.

7. Surgical Treatment

With the widespread clinical application of CT, diagnosing hypertensive cerebral hemorrhage has become swift and accurate. With advancements in microsurgery and stereotactic surgery, surgical accuracy has improved, greatly reducing trauma to brain tissue, broadening the indications for hypertensive cerebral hemorrhage surgery.

Generally, the hematoma forms within 6 hours of onset, with edema peaking 8～24 hours later. Clearing the hematoma before this period may yield better functional recovery. Early surgery not only clears the hematoma promptly, resolving intracranial hypertension, but also reduces damage from blood decomposition products on brain tissue, playing a crucial role in reducing mortality and disability rates.

(1) Surgical indications: There are currently no uniform standards for surgical indications in treating hypertensive cerebral hemorrhage. Generally, age is not a limiting factor if vital organs function well and there are no serious complications such as deep coma, gastrointestinal bleeding, decorticate rigidity, bilateral pupil constriction, or central hyperthermia. Indications include: ① Hemorrhage volume over 20ml. ② Thalamic or basal ganglia hematoma. ③ Hematoma extending into the ventricles affecting cerebrospinal fluid circulation should be drained early via ventricular puncture, combined with daily lumbar puncture releasing 10～20ml of cerebrospinal fluid until stable, maintaining drainage for about a week under strict sterile conditions. ④ Hematomas involving the brainstem, elderly patients, or brain herniation are unsuitable for surgery. ⑤ Preoperative high blood pressure can be lowered first. ⑥ Vascular malformations or ruptured aneurysms should be carefully evaluated. ⑦ Cerebellar hemisphere hemorrhage volume around 20ml. ⑧ No improvement with conservative medical treatment, progressively worsening condition, or early signs of brain herniation.

(2) Timing of surgery: Previously, it was believed that early-stage cerebral hemorrhage patients were critically ill, with high surgical risks and potential for rebleeding, thus surgery was performed after 24 hours. Recent studies show that hypertensive cerebral hemorrhage generally forms a hematoma within half an hour, with surrounding edema forming within 3 hours, stopping bleeding and appearing within 6～7 hours, nearby brain tissue necrosis and irreversible damage occurring, moderate edema at 12 hours, and severe edema at 24 hours. Therefore, most scholars advocate early or ultra-early surgery within 6～8 hours of onset to precede the development of edema around the hematoma, relieving pressure on brain tissue and preventing brain edema, breaking the vicious cycle caused by red blood cell decomposition and a series of secondary changes, improving survival rate and quality of life. Surgery within 3 days of bleeding is generally suitable. Whether puncture should be performed more than 20 days after bleeding depends on specific circumstances.

(3) Surgical methods: Common hematoma removal methods include: ① Neuroendoscopic treatment technology; ② Minimally invasive surgery for hypertensive cerebral hemorrhage; ③ Craniotomy or craniectomy hematoma removal; ④ CT-guided stereotactic aspiration; ⑤ Ventricular drainage, hematoma dissolution.

8. Recovery Phase Treatment for Cerebral Hemorrhage

The purpose of recovery phase treatment is to promote functional recovery of paralyzed limbs and language disorders, improve brain function, reduce sequelae, and prevent recurrence. Recovery treatment timing is when the cerebral lesion is basically stable, cerebral edema and intracranial hypertension symptoms subside, and damaged brain function gradually recovers. During this phase, besides original internal medicine treatments, emphasis should be on improving cerebral blood circulation and promoting nutritional metabolism, gradually selecting drugs that dilate cerebral vessels. Drug action should be gentle, starting with low doses and gradually increasing to therapeutic levels, possibly increasing the variety of drugs step by step. Another important treatment measure during the recovery phase is rehabilitation therapy, especially for patients with severe neurological deficits such as hemiplegia or aphasia, starting early and proceeding systematically for better results and significantly reducing disability.

(1) Preventing Rebleeding: Recurrent cerebral hemorrhage is one of the main causes of death and disability among survivors of cerebrovascular diseases. Song Deren et al. reported that the interval between recurrent cerebral hemorrhages ranges from 3 months to 5 years, accounting for 19.5% (58/297) of simultaneous cerebral hemorrhages. 37.9% recur within a year of the first episode, 75.8% within two years, and 93% within three years, meaning most patients recur within three years.

Regarding the inducements of rebleeding, Passeros et al.'s combined variable analysis showed that risk factors for recurrent cerebrovascular disease are not significantly related to age, gender, hyperlipidemia, smoking, heavy drinking, or diabetes, but rather uncontrolled hypertension and vascular amyloidosis.

Song Deren et al.'s research found that the main inducement of rebleeding is hypertension, followed by emotional changes such as excitement or sadness, diabetes. Elderly patients with rebleeding often have a history of transient ischemic attacks or ischemic cerebrovascular disease, fewer cases of hyperlipidemia rebleeding. Therefore, actively controlling hypertension, reasonably treating diabetes, paying attention to emotional self-regulation, living a regular life, eating moderately, and promptly treating constipation are important aspects in preventing recurrent cerebral hemorrhage. Regarding the outcome of rebleeding, Song Deren et al. reported that all 58 cases were treated internally, with 29 cases improving and 29 dying, each accounting for 50% of the total number of patients.

(2) Drug treatment:

① Calcium channel blockers: After cerebral hemorrhage, the surrounding brain tissue is ischemic and hypoxic, with neural cells in a state of calcium overload. Using calcium channel blockers can alleviate calcium overload, prevent cell death, improve cerebral microcirculation, and increase cerebral blood flow supply. Common drugs include Nimodipine (Nidal), 20～40mg, three times a day; or Nimodipine (Nimotop), 30mg, three times a day; Clemastine (Cinnarizine), 25mg, three times a day. Use with caution in cases of low blood pressure, significant cerebral edema, and increased intracranial pressure.

② Cerebral metabolic activators: Promoting neuro-metabolic drugs such as Piracetam (Nootropil), Cytidine Diphosphate Choline (CDP-Choline), Cerebrolysin, Gamma-Aminobutyric Acid (GABA), Coenzyme Q10, B vitamins, vitamin E, and vasodilator drugs can be selected. Herbal formulas for activating blood circulation and removing blood stasis, invigorating qi and unblocking meridians can also be chosen.

(3) Dietary Control:

① Provide nutritious and easily digestible foods to meet the body's protein, vitamin, mineral, and total caloric needs.

② Drink plenty of water and consume semi-solid foods regularly. Due to concerns about excessive urination, paralyzed patients may try to minimize water intake, which is detrimental. Meals should include both food and soup, especially porridge, which is ideal. Eating some pickled vegetables can encourage drinking more water. For those unwilling to drink water, consuming juicy fresh fruits can help prevent constipation and urinary tract infections.

③ Pay attention to dietary fiber intake. Food should not be overly refined to prevent constipation. Avoid strong tea, alcohol, coffee, and spicy stimulating foods.

④ Control salt and cholesterol intake, increasing foods rich in B vitamins.

(4) Rehabilitation Treatment:

① Passive Movement and Massage: When the patient's limb lacks strength, passive movement should be the primary focus. Movements should be delicate and gentle, rhythmically addressing each joint to ensure full range of motion across all joints. Perform twice daily, three rounds each time. This maintains joint and soft tissue mobility, preventing contractures that restrict movement, while joint contractures can cause local circulatory disturbances, complicating rehabilitation. As the patient regains limb function, gradually transition to a combination of active and passive movements. Special attention should be paid to external rotation and abduction activities of the affected shoulder joint to prevent shoulder joint contracture and pain.

② Active Movement: Once the patient's limb gains strength, active movement should begin promptly.

Bed-based Active Movement and Sitting Training: Some stroke patients initially perceive their entire body as paralyzed, not just one side, feeling entirely powerless. Overcoming this involves helping the patient learn to use their healthy side to move their body in bed, while simultaneously performing extension and flexion exercises in the supine position. Being conscious, the patient should start raising the head of the bed early. When tolerable, sitting in bed allows for limb function training, such as pulling ropes or objects, practicing sit-ups, stretching tight muscles to increase activity range.

Bedside Training: Gradually enable the patient to sit up at the bedside. The method involves curling the healthy side, placing the healthy leg beneath the affected leg, lowering the affected leg over the edge of the bed, and using the healthy arm to support themselves while sitting up. This utilizes visual input and proprioceptive input from the healthy arm for learning and training balance in the seated position. Learning seated balance makes standing balance easier.

Standing Training: After bedside training, create conditions for independent standing with crutches or leaning against walls, eventually enabling indoor and outdoor mobility.

③ Physical Therapy and Acupuncture.

④ Medical Sports Therapy: Coordination results from frequent and repeated training. After paralysis, coordination is lost. Therefore, before completing complex coordinated movements, the ability to execute each simple decomposed action must be acquired. Only through gradual progression from simple to complex, persistent repetition can these muscles become part of normal activities. Progressively improving each muscle group through active-assisted, active, active against gravity, and resistance exercises enables gradual limb function coordination through multiple repetitions of physical exercise.

9. Stroke Unit Treatment Model for Cerebrovascular Diseases

(1) What is a Stroke Unit: A stroke unit is a stroke treatment management model that provides systematic drug treatment, physical rehabilitation, language training, psychological rehabilitation, and health education for stroke patients. Core staff members include clinical doctors, specialized nurses, physical therapists, occupational therapists, speech therapists, and social workers.

From the above concept, the characteristics of a stroke unit can be summarized as:

① Targeting hospitalized stroke patients, it is neither an emergency green channel nor comprehensive stroke management but rather management during the hospital stay.

② A stroke unit is not a therapy but a ward management system that does not include new treatment methods.

③ This new ward management system should be a multidisciplinary care system.

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