Objective: To reduce the blood pressure and elevate intracranial pressure using nimodipine (Nimotop Intravenous (IV) infusion). Thus, intracerebral hemorrhage was controlled, and the purpose of hemostasis was achieved. Methods: Sixty-eight patients with intracerebral hemorrhage were divided into a treatment group (n = 51), and a control group (n = 35). Nimotop solution (10 mg) was administered as a fast-flowing IV infusion in the treatment group, and 250 ml 20% mannitol infusion was given to patients in the control group twice every day. Patients in both groups received treatment for seven days, and the blood pressure on the treatment day was measured. A brain Computed Tomography (CT) scan was performed as a reexamination within two weeks. Results: The blood pressure in the treatment group was decreased from 179/104 to 151/91 mmHg, averagely, and in the control group was decreased from 181/108 to 180/103 mmHg, averagely. The difference between these two groups was statistically significant ( <i> P </i> < 0.01). Hematoma enlargement occurred in 20 patients (53.3%) in the treatment group, and four patients in the control group (8.57%). The difference between both groups was statistically significant ( <i> P </i> < 0.01). There were eight deaths in the treatment group. Seven deaths were caused by cerebral hernia, and one was caused by complications. There was one death in the control group caused by lung infection and gastrointestinal bleeding. Conclusion: Nimodipine can dilate the arteries, reduce blood pressure, and elevate intracranial pressure, lowering pressure gradients across vessel wall which destroy the vessel wall. Also, nimodipine can prevent hemorrhage as well as recurrent hemorrhage, and can used as the first choice of rescue drug. What ’ s more, dehydration drugs such as mannitol should not be used in the early stage of intracerebral hemorrhage in order to prevent hematoma enlargement.
Nimodipine (Nimotop IV infusion) is widely used to treat cerebral vasospasm and cerebral infarction after subarachnoid hemorrhage [
Subjects in the study were all patients treated in the Emergency Department of our hospital who met the following criteria: 1) acute hypertensive intracerebral hemorrhage, 2) within 24 hours of the onset of symptoms, 3) consciousness without coma, 4) quantitative estimation of hematoma was performed, and location of hematoma was identified using CT scan. Patients who met at least one of the following criteria were excluded from the study: 1) a systolic blood pressure < 100 mmHg; 2) gastrointestinal bleeding; 3) obvious liver dysfunction; 4) coma. Subjects were randomly assigned to two groups. There were 51 patients (33 males and 18 females) aged 45 to 84 years, with a mean age of 64 ± 11 years old in the treatment group. There were 35 patients (26 males and 9 females) aged 36 to 79 years, with a mean age of 60 ± 11 years old in the control group.
In the Emergency Department, two groups underwent blood pressure measurement, physical examination and brain CT scans. Nimodipine (10 mg) was added into 500 ml 10% glucose water, and was administered via IV infusion over 3 to 10 hours in the patients in the treatment group. The infusion was performed 1 to 2 times per day, and lasted 7 days. In the control group, 250 ml 20% mannitol infusion was administrated every 8 h (q8h) or q12h every day. The infusion lasted for 7 days, and was finished within half an hour. In addition, an intramuscular injection of reserpine (1 - 2 mg) was given to patients whose systolic blood pressure was more than 180 mmHg. Apart from the above differences in the two groups, patients in both groups were given 16 g 6-aminocaproic acid, nutritional agents for neurons and other drugs at the same time within 7 days. Mannitol or furosemide could be given for dehydration to comatose patients in the treatment group within 12 hours after the onset of symptoms in order to reduce intracranial pressure and ensure cerebral perfusion pressure. Blood pressure measurement was performed twice every day in both groups. Within two weeks, brain CT scans were performed as a reexamination in order to assess hematoma changes, and the time of onset, the first treatment and two CT scans was recorded.
First: Changes in blood pressure on the first day before and after treatment were used to determine the clinical efficacy.
Second: Changes in hematoma volumes detected by two brain CT scans were used to determine the changes in intracerebral hematoma volumes.
Changes in the blood pressure and hematoma volumes before and after treatment were examined using a t or t’ test, and hematoma location and expansion rates were examined using a chi-square test.
Hematoma locations: there were 26 patients with putaminal hemorrhage, 12 with thalamic hemorrhage, 4 with lobar hemorrhage, 5 with brainstem hemorrhage, and 4 with cerebellar hemorrhage in the treatment group. There were 23 patients with putaminal hemorrhage, 6 with thalamic hemorrhage, 2 with brainstem hemorrhage, 3 with lobar hemorrhage, and 1 with cerebellar hemorrhage in the control group. The chi-square test performed on the hematoma locations in both groups showed a P value larger than 0.05, indicating that there were no significant differences.
The time from the onset to the first CT scan and from the first CT scan to the second CT scan in the two groups (
Blood pressure changes on the first day of treatment in the two groups (
Comparison of hematoma volumes in the two groups was detected by CT scan ( x ¯ ± s ml) (
There were eight deaths in the control group, of which seven deaths were caused cerebral hernia, and of which one death was caused by hyperpyrexia and pulmonary infection on the day 9. There was one death in the treatment group. The patient died from pulmonary infection, hyperpyrexia, and gastrointestinal bleeding on the fifteenth day of the disease.