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

Medical Treatment for Brain Hemorrhage (Part 3) - Western Medicine Treatments

1. Principles of Drug Therapy for Acute Brain Hemorrhage

- Prevent further bleeding.

- Reduce intracranial pressure.

- Control cerebral edema.

- Maintain vital functions and prevent complications.

Specific measures:

(1) Bed rest: Elevate the head of the bed, minimize moving the patient. Typically bed rest lasts about 3-4 weeks.

(2) Ensure airway patency: The first 5 minutes after a brain hemorrhage are critical for life. Ensure airway is clear by loosening collars, removing dentures, placing the patient in a lateral position, tilting the head back to facilitate secretion drainage, and promptly clearing oral vomit. If asphyxiation occurs, immediately clean the mouth and perform artificial respiration.

(3) Rational use of sedatives: Administer sedatives, antispasmodics, and analgesics for agitated or epileptic patients.

(4) Adjust blood pressure: For high blood pressure cases, use small doses of Labetalol (Reserpine) or intramuscular injection of 25% Magnesium Sulfate 10ml; conscious patients may be given oral antihypertensive drugs.

(5) Minimize movement: If the patient is in a confined space, quickly move them to a more spacious area while minimizing head vibrations and maintaining a horizontal head position to avoid airway obstruction.

(6) Internal medicine treatment: Small hematomas with no significant increase in intracranial pressure can be managed primarily with basic internal medicine treatments, sometimes early introduction of drugs to improve cerebral circulation, often using traditional Chinese medicine formulations that promote blood circulation and remove blood stasis. Patients with cerebral edema and increased intracranial pressure require active and rational dehydration therapy.

(7) Surgical treatment: Large hematomas with significant midline shift usually require timely surgery. Emergency surgery might be necessary for critically ill patients. Early surgery within 6 hours of onset can maximize reduction of secondary damage, improving survival rates and reducing disability rates.

(8) Hemostatic agents: Commonly used are Etamsylate (Hemocoagulase), Tranexamic Acid (Antifibrinolytic Fumaric Acid), Vitamin K, etc. Dosages should not be excessive, and variety limited.

(9) Strengthened nursing care to maintain airway patency: Regular turning and back tapping, preventing pneumonia and bedsores. Vital signs including consciousness, pupils, blood pressure, pulse, and respiration should be monitored every half hour, then every 2-4 hours once stable, with detailed records kept.

(10) Timely rescue: If consciousness worsens or agitation increases, unequal pupil sizes, delayed light reflex, slow pulse, elevated blood pressure, indicating herniation, immediate rescue is required.

2. General Treatment During the Acute Phase

(1) Maintain airway patency: Comatose patients should be placed on their side, avoiding supine positions to prevent tongue base posterior displacement obstructing the airway. Regularly turn and tap the back to help cough up phlegm, frequently suction secretions, or use nebulization to humidify phlegm. Tracheotomy should be performed if respiratory obstruction occurs to prevent oxygen deprivation exacerbating cerebral edema. Oxygen mixed with 5% CO2 can be administered intermittently, avoiding prolonged pure oxygen inhalation which may cause cerebral vasospasm or oxygen poisoning.

(2) Maintain nutrition and electrolyte balance: Usually fasting for the first 1-2 days is recommended, daily fluid intake should be around 1500-2000ml, monitoring input-output balance. Dehydration agents require careful potassium supplementation. Additionally, acidosis, non-ketotic diabetes, hyperosmolar coma should be prevented and corrected. Nasogastric feeding can start from day 3 for comatose or unable-to-eat patients to ensure nutritional supply. Fluid intake should be appropriately restricted, generally not exceeding 2500ml daily, with adjustments based on fever, vomiting, sweating, diuretics, etc. Avoid high-sugar fluids; consider fat emulsion, human albumin, amino acids, or energy mixtures when necessary.

3. Blood Pressure Adjustment

The principle of early blood pressure reduction for hypertensive brain hemorrhage patients is:

(1) Carefully evaluate blood pressure lowering indications. Generally, when systolic blood pressure exceeds 24-26.66kPa (180-200mmHg), appropriate blood pressure reduction can be considered to prevent further bleeding, but caution is needed for patients with large pulse pressures.

(2) Blood pressure control should be smooth, making "peaks" and "valleys" in 24-hour blood pressure close. Rapid blood pressure reduction should be avoided, as well as repeated, large amounts, or combined use of multiple potent antihypertensive drugs. Commonly used Reserpine 0.5-1mg intramuscular injection, 25% Magnesium Sulfate 10mg deep intramuscular injection, repeatable every 6-12 hours. Other oral antihypertensive drugs or diuretics can also be used, but strong vasodilators should be cautiously used or avoided. When patients show no sensitivity to blood pressure reduction, it may indicate increased intracranial pressure.

(3) Blood pressure reduction should not be too rapid. A feasible method is gradually lowering blood pressure over a period to an appropriate level or slightly higher without symptoms of cerebral ischemia. Most recommend stabilizing blood pressure around 20-21.33/12-13.33kPa (150-160/90-100mmHg), ideally maintaining it slightly above 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, rapid blood volume reduction, and water-electrolyte disorders must be taken seriously.

(5) When using antihypertensive drugs, observe changes in blood pressure. Raise the head of the bed approximately 30-45 degrees if blood pressure is too high. Lower the bed when blood pressure approaches normal. If blood pressure remains persistently low, online appointment registration should be made to appropriately use pressor drugs to maintain the aforementioned levels.

4. Control Cerebral Edema

Reducing intracranial pressure is a crucial step in preventing brain herniation. After brain hemorrhage, cerebral edema gradually worsens, typically starting around 6 hours post-hemorrhage, peaking at 3-4 days, and gradually subsiding after two weeks. The result of cerebral edema is increased intracranial pressure, potentially leading to brain herniation. Therefore, controlling cerebral edema and intracranial hypertension is key to reducing mortality rates. Immediate and active measures should be taken to control cerebral edema.

Clinical indicators suggest using dehydration agents via intravenous or intramuscular injection unless the patient is conscious, has mild intracranial pressure elevation, and no vomiting, allowing oral medication. In cases of difficulty with intravenous or oral administration, rectal drip with 20% Glycerol or 30% Mannitol can be considered. In severe dehydration with intracranial hypertension, carotid artery injection of 40-60ml Mannitol can achieve cerebral tissue dehydration with minimal systemic effects. Selection of dehydration agents and dosages should be based on the degree of intracranial pressure elevation and overall condition such as heart and kidney function. In deeply comatose patients or those showing early signs of brain herniation, strong dehydration agents should be used. Typically, 2-3 types should be alternated, such as 20% Mannitol, Furosemide (Lasix), Glycerol preparations. Heart or kidney dysfunction patients often need to use Furosemide first. Colloid solutions like 20% or 25% Human Albumin can prevent reduced blood volume and hypotension.

Early application of adrenal corticosteroids helps reduce cerebral edema. Among corticosteroids, Dexamethasone shows the strongest anti-cerebral edema effect, especially for vasogenic cerebral edema. Common dosage is 10-15mg added to glucose solution or mannitol, intravenously dripped, reducing and stopping over 1-2 weeks. Since corticosteroid action is relatively slow, and brain hemorrhage patients prone to gastrointestinal bleeding and lung infections may worsen or mask conditions due to corticosteroid use, plus slow intracranial pressure reduction and inability to rapidly counteract cerebral edema, routine use is not recommended, especially for diabetic, hypertensive, or ulcerative disease patients who should use cautiously or avoid. Concurrent use of gastric mucosa protective drugs is advised to prevent stress-induced gastric bleeding.

5. Application of Hemostatic Agents

Whether hemostatic agents should be used in brain hemorrhage patients remains controversial. Various hemostatic agents mainly stop capillary bleeding or seepage in brain substance, with uncertain effects on arterial rupture bleeding.

Blind use of hemostatic agents in patients with atherosclerosis could increase the risk of ischemic cerebrovascular disease, myocardial infarction, or renal artery thrombosis. Thus, some oppose their use. Hemostatic agents can be used for gastrointestinal bleeding patients under regular coagulation function checks and short-term use under laboratory supervision. For intraventricular or subarachnoid hemorrhage patients, appropriate hemostatic drugs can be considered to prevent rebleeding.

6. Artificial Hibernation Cooling Therapy

Artificial hibernation cooling therapy reduces the brain's basal metabolic rate, decreases oxygen consumption, increases tolerance to hypoxia, improves hypoxic state, reduces cerebral edema, lowers intracranial pressure, protects brain tissue, and reduces or avoids rebleeding.

(1) Early cooling: Ideally within 6 hours of onset, beyond 7-8 hours brain protection effect is poorer. Cooling time should not exceed 48 hours, extendable if concurrent high fever occurs.

(2) Cooling methods: Many cooling methods exist, advanced low-temperature rooms are beneficial. If resources are limited, methods like ice caps on the head + ice packs on major arteries + drugs can be used.

(3) Gradual rewarming principle: First stop medication, then remove ice packs, finally remove the ice cap, completing within 8-12 hours. Short-term low temperature rarely causes complications, though muscle tremors and agitation may occur, treatable with Atracurium 25mg or Diazepam 10mg.

7. Surgical Treatment

With the widespread clinical use of CT, diagnosis of hypertensive brain hemorrhage has become swift and accurate. With developments in microsurgery and stereotactic surgery, surgical precision has improved, greatly reducing trauma to brain tissue, expanding surgical indications for hypertensive brain hemorrhage.

Generally, hematoma forms within 6 hours of onset, reaching peak edema 8-24 hours post-bleeding. Clearing hematoma before this can yield better functional recovery. Early surgery not only promptly removes hematoma and addresses intracranial hypertension, but also reduces destruction of brain tissue by blood breakdown products, significantly decreasing mortality and disability rates.

Surgical indications include patients not particularly old, with good organ function, no severe complications like deep coma, gastrointestinal bleeding, decorticate rigidity, bilateral pupil constriction, central hyperthermia, and meeting one of the following criteria:

① Hemorrhage volume over 20ml.

② Thalamic or basal ganglia hematoma.

③ Ventricular rupture affecting cerebrospinal fluid circulation requiring early ventricular puncture drainage, with lumbar puncture once daily, releasing 10-20ml cerebrospinal fluid until stable, maintaining drainage tube for about a week under strict sterile operation.

④ Hematoma involving brainstem, elderly, or brain herniation unsuitable for surgery.

⑤ Preoperative blood pressure too high requiring initial blood pressure reduction.

⑥ Vascular malformation or aneurysm rupture requires caution.

⑦ Cerebellar hemisphere hemorrhage volume around 20ml.

⑧ Conservative medical treatment showing no improvement, worsening condition, or early signs of brain herniation.

Selection of surgical timing: Previously, people believed early brain hemorrhage patients were critically ill, posing high surgical risks with potential rebleeding, suggesting surgery after 24 hours. Recent studies show hypertensive brain hemorrhage typically forms hematoma within half an hour, perihematoma edema forming within 3 hours, bleeding stopping and perihematoma edema appearing within 6-7 hours, irreversible damage to adjacent brain tissue occurring, moderate edema within 12 hours, and severe edema within 24 hours. As research progresses, most scholars advocate early or ultra-early surgery, performing surgery within 6-8 hours of onset to precede perihematoma brain tissue edema, alleviating hematoma compression and preventing cerebral edema, breaking the vicious cycle of hematoma decomposition, cerebral tissue edema, and other secondary changes, improving survival rate and quality of life. Surgery within 3 days post-bleeding is generally recommended. Whether puncture should be performed after more than 20 days depends on specific circumstances.

Common hematoma removal surgical methods include:

① Neuroendoscopic treatment technology.

② Minimally invasive surgery for hypertensive brain hemorrhage.

③ Craniotomy or bone flap hematoma removal.

④ CT-guided stereotactic aspiration.

⑤ Ventricular drainage, hematoma dissolution.

8. Recovery Period Treatment for Brain Hemorrhage

The goal of recovery period treatment is to restore paralyzed limbs and language impairments, improve brain function, reduce sequelae, and prevent recurrence. Recovery treatment begins when brain lesions stabilize, cerebral edema and intracranial hypertension symptoms subside, and damaged brain function gradually recovers. During this phase, besides original internal medicine treatment, focus should be on improving cerebral circulation and promoting nutrition metabolism, gradually selecting vasodilator drugs. Drug effects should be gentle, starting with low doses, gradually increasing to therapeutic doses, possibly increasing drug varieties. An important treatment measure during recovery is rehabilitation treatment, especially for severely affected patients with hemiplegia, aphasia, etc., starting early and progressing systematically yields better results, significantly reducing disability.

(1) Prevent Rebleeding: Recurrent brain hemorrhage is a major cause of death and disability among stroke survivors. Domestic studies report recurrent intervals ranging from 3 months to 5 years, accounting for 19.5% (58/297) of simultaneous brain hemorrhages. Within one year of the first episode, 37.9% recur, 75.8% within two years, and 93% within three years, meaning most patients recur within three years.

Regarding rebleeding triggers, Passeros et al. found through multivariable analysis that risk factors for recurrent cerebrovascular disease had no significant relation to age, gender, hyperlipidemia, smoking, heavy drinking, or diabetes, but rather uncontrolled hypertension and vascular amyloidosis.

Domestic studies conclude that hypertension is the main trigger for rebleeding, followed by emotional changes like excitement or sadness, diabetes. Elderly rebleeding patients often have TIA or ischemic cerebrovascular disease history, fewer rebleeding cases with hyperlipidemia. Therefore, actively controlling hypertension, reasonably treating diabetes, regulating emotions, living regularly, eating moderately, and timely treating constipation are important steps in preventing recurrent brain hemorrhage. Regarding rebleeding outcomes, Song Derugen reported all 58 cases received internal medicine treatment, 29 improved, 29 died, each accounting for 50% of patients.

(2) Drug Treatment:

① Calcium Channel Antagonists: After brain hemorrhage, surrounding brain tissue experiences ischemia and hypoxia, with neurons in calcium overload state. Using calcium channel antagonists 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 daily; Nimodipine (Nimotop) 30mg, three times daily; Cinnarizine (Cerebrolizin) 25mg, three times daily. Use cautiously in cases of low blood pressure, obvious cerebral edema, and increased intracranial pressure.

② Cerebral Metabolic Activators: Promote nerve metabolism drugs such as Piracetam (Cerebrolysin), Citicoline (Cytidine Diphosphate-Choline), Cerebroprotein Hydrolysate (Cerebrolysin), Gamma-Aminobutyric Acid, Coenzyme Q10 (CoQ10), B vitamins, Vitamin E, and vasodilator drugs, or select prescriptions that activate blood circulation and remove blood stasis, tonify qi and promote blood circulation.

(3) Dietary Control:

① Provide nutrient-rich and easily digestible foods to meet protein, vitamin, mineral, and total caloric needs.

② Drink plenty of water and eat semi-fluid foods. Paralyzed patients often fear frequent urination and limit water intake, which is detrimental. Diets should include meals and soups, especially porridge, and some pickles to encourage water intake. For those reluctant to drink water, consume juicy fresh fruits to prevent constipation and urinary tract infections.

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

④ Control salt and cholesterol intake, increase 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 main focus. Movements should be gentle and gradual, rhythmically working through all joints to ensure full range of motion. Perform twice daily, three rounds each time, to maintain joint and soft tissue mobility, prevent restricted movement due to contracture, and avoid local circulatory impairment. When the patient's limb regains function, gradually transition to active and passive movements combined. Pay special attention to external rotation and abduction of the affected shoulder joint to prevent contracture and pain.

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

Bed exercises and sitting training: Some stroke patients initially perceive complete paralysis, feeling completely powerless. Overcoming this perception involves helping patients learn to use their healthy side to move their body in bed, simultaneously performing supine limb flexion and extension exercises. Patients, being conscious, should elevate the bedhead early. When tolerable, perform limb function exercises while seated in bed, such as pulling ropes or objects, practicing sit-ups, stretching hands and lifting legs to forcefully stretch tight muscles, increasing range of motion.

Edge-of-bed exercises: Gradually teach patients to sit at the edge of the bed. The method involves curling the healthy side, placing the healthy leg under the affected leg, lowering the affected leg off the bed, and supporting themselves with the healthy arm. This allows visual input and proprioceptive input from the healthy arm to enhance learning and training of sitting balance. Once sitting balance is learned, standing balance becomes easier.

Standing exercises: After successful edge-of-bed exercises, create conditions for independent standing with crutches or against the wall, eventually walking indoors and outdoors.

③ Physical therapy and acupuncture treatment.

④ Medical sports therapy: Coordination results from frequent and repetitive training. When paralysis occurs, coordination is lost. To perform complex coordinated movements, each simple component must be mastered. Only through gradual progression from simple to complex, persistent repetition, can these muscles become part of normal activity. Through active-assisted, active, active-against-gravity, and active-resistance exercises, each muscle group progresses from simple to complex, improving limb function through repeated 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 providing systematic drug treatment, physical rehabilitation, language training, psychological rehabilitation, and health education for stroke patients. Core staff include clinical doctors, specialized nurses, physical therapists, occupational therapists, speech therapists, and social workers.

Key features of Stroke Units:

① Focuses on hospitalized stroke patients, not an emergency green channel or comprehensive stroke management, but management during hospitalization.

② Stroke units are not a therapy but a ward management system without new treatment methods included.

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