Liver dysfunction in spontaneous intracerebral hemorrhage

The purpose of this study was to investigate the relationship between mild degrees of liver dysfunction and spontaneous intracerebral hemorrhage (ICH) from the hemostatic standpoint. A detailed study of hemostatic systems was made in 462 patients with ICH. To compare ICH with the other cerebrovascular diseases, data from 120 patients with subarachnoid hemorrhage and 114 others with cerebral infarction were reviewed. At admission, the medical histories of the patients, including information about previous alcohol consumption, was taken, and blood samples were collected to perform the following studies: platelet count, fibrinogen level, prothrombin time, activated partial thromboplastin time, antithrombin III, plasminogen and alpha 2-antiplasmin activity, platelet aggregability, and liver function tests. The incidence of liver dysfunction and alcohol consumption in patients with ICH was significantly (P < 0.05) higher than in patients with subarachnoid hemorrhage and in those with cerebral infarction. Hematoma volume, mortality rate, and past alcohol consumption in patients with ICH significantly increased with worsening severity of liver dysfunction. Although almost all hemostatic parameters became worse with increasing severity of liver dysfunction, they changed within the normal limits. Platelet aggregability and alpha 2-antiplasmin activity in patients with liver dysfunction were remarkably deteriorated beyond normal limits. In conclusion, liver dysfunction associated with alcohol consumption appears to be an important factor in the deterioration of the clinical status of patients with ICH and may be one of the causative factors in the development of ICH. Although mildly impaired hemostatic systems may be partially responsible for these adverse effects of liver dysfunction on ICH, it seems probable that nonhemostatic mechanisms are attributed to the effects.     

Prognostic factors in spontaneous intracerebral hemorrhage

The introduction of etiological, diagnostic and therapeutical factors have modified the knowledge on the evolutive behaviour of spontaneous intracerebral hemorrhages (ICH). Mortality and morbidity associated to spontaneous ICH were assessed using as independent variables clinical and neuroimage factors obtained upon admission of the patients. We studied 228 patients with spontaneous ICH selected from a data bank of 277 patients with non-traumatic ICH. During the first 24 hours, we assessed several clinical factors (arterial hypertension, Glasgows Neurological Scale and Barthels Scale) and TC images (size, location, extension of bleeding to ventricles, edema and atrophy). Thirty-one per cent of the patients died during the first 2 months. The multiple linear regression study showed that mortality was related to variables of the Glasgows Neurological Scale upon admission, extension to ventricles, size of ICH and perilesional edema, whereas the morbidity was only related to the size of the hemorrhage. Severity of the clinical affection, extension of the bleeding to ventricles, size of the hemorrhage and presence of perilesional edema, but not arterial hypertension, were the main factors affecting mortality at two months of spontaneous ICH.     

C-type hepatitis in spontaneous intracerebral hemorrhage

The prevalence of hepatitis C virus (HCV) in 139 cases of spontaneous intracerebral hemorrhage (ICH) was investigated with regard to a diagnosis of hypertension. Patients under 30 and over 79 years of age were omitted from this study, and those with complicating malignancies and undergoing anti-coagulation or antiplatelet therapy were also excluded. The prevalence of HCV was significantly higher among the ICH group as a whole (19 out of 139 cases, p < 0.05) especially in the non-hypertensive group (7 out of 29 cases, p < 0.01), compared to the control group (7 out of 140 cases without ICH). The non-hypertensive HCV-positive group (7 cases) had significantly higher GOT and GPT levels, prolonged PT and a-PTT values, and lower platelet counts, compared to the hypertensive HCV-negative group (74 cases). The HCV antibody titers did not differ among the HCV-positive groups. The results suggest that chronic hepatitis due to HCV infection is a major risk factor for spontaneous intracerebral hemorrhage, especially in non-hypertensive patients.     

Prevalence of risk factors in spontaneous intracerebral hemorrhage and aneurysmal subarachnoid hemorrhage

OBJECTIVE: To evaluate whether differences exist in the occurrence of modifiable risk factors between aneurysmal subarachnoid hemorrhage and spontaneous intracerebral hemorrhage, since these stroke subtypes have frequently been combined in epidemiological studies and labeled hemorrhagic stroke. DESIGN: Cross-sectional survey. SETTING: Helsinki University Central Hospital in Helsinki, Finland. PATIENTS: One hundred fifty-six consecutive patients with spontaneous intracerebral hemorrhage aged 16 to 60 years (96 males and 60 females) and 281 patients with aneurysmal subarachnoid hemorrhage (145 males and 136 females) who were admitted to an emergency department. MAIN OUTCOME MEASURES: Prevalence of several health habits, previous diseases, and medication of patients with spontaneous intracerebral hemorrhage were compared with that of patients with subarachnoid hemorrhage using multiple logistic regression. RESULTS: Hypertension (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.6-4.3), diabetes mellitus (OR, 26.4; 95% CI, 3.1-221.6), alcohol intake within the preceding week (for 1-150 g of alcohol: OR, 2.0; 95% CI, 1.1-3.6; for 151-300 g of alcohol: OR, 1.7; 95% CI, 0.8-3.8; and for > 300 g of alcohol: OR, 4.4; 95% CI, 2.1-9.1), and anticoagulant treatment (OR, 21.8; 95% CI, 2.3-207.3) were all significantly more common, but current cigarette smoking (OR, 0.3; 95% CI, 0.2-0.5) was less common in patients with intracerebral hemorrhage than in those with subarachnoid hemorrhage simultaneously after adjustment for sex, age, and body mass index. In males, hypertension (OR, 2.3; 95% CI, 1.1-4.5) and alcohol intake (for > 300 g/wk: OR, 5.8; 95% CI, 2.2-15.7) were more common, but current smoking (OR, 0.2; 95% CI, 0.1-0.4) was less common in patients with intracerebral hemorrhage than in those with subarachnoid hemorrhage after adjustment for age, body mass index, and diabetes mellitus. In females, hypertension (OR, 2.9; 95% CI, 1.4-5.8) and anticoagulant treatment (OR, 10.0; 95% CI, 1.0-100.2) were more common in patients with intracerebral hemorrhage after adjustment for age and body mass index. In univariate statistics, patients with intracerebral hemorrhage were also older, more often had previous symptoms of cerebral ischemia, and had higher values for body mass index and gamma-glutamyltransferase than did those with subarachnoid hemorrhage. CONCLUSIONS: Hypertension, diabetes mellitus, anticoagulant treatment, and amount of alcohol taken within 1 week seem more commonly to be associated with intracerebral hemorrhage than with subarachnoid hemorrhage, which is, however, associated more frequently with cigarette smoking.     

Specific strategies in the treatment of young and middle-age patients with spontaneous intracerebral hemorrhage

The paper is based on the analysis of 235 young and middle-age patients with non-traumatic cerebral hemorrhage. Tactics of treatment is determined for each group depending on bleeding localization in accordance with World Health Organization's classification (1981). Operative treatment is recommended for lateral site of hematomas of 25 cm3 and more signs of media structures dislocation of 5 mm and more. With the development of hypertension-hydrocephal syndrome surgical intervention is directed at its elimination and where possible at hematoma's ablation. The amount of operative interventions is limited in case of medial and mixed variants of hemorrhages especially when bleedings affect mesencephal structures. In conditions of a neurosurgical clinic a pharmacotherapy is used as an independent one, as a preparation for surgical treatment as well as during operation and in postoperative period.     

Computed tomography in intracerebral hemorrhage

Computed tomography is a practical and simple procedure for diagnosis of acute intracerebral hemorrhage. By this means, operable intracerebral hemorrhage was diagnosed in five patients; four were treated surgically. Computed tomography showed the size and location of the hematomas, making surgical treatment feasible despite occasional large extensions of the lesions.     

Management of hypertension in acute intracerebral hemorrhage

Hypertension commonly occurs in the acute period following spontaneous intracerebral hemorrhage. Management of this hypertension is controversial. Some advocate lowering blood pressure to reduce the risk of bleeding, edema formation, and systemic hypertensive complications, whereas others advocate allowing blood pressure to run its natural course as a protective measure against cerebral ischemia. This article reviews the pertinent clinical and experimental data regarding these issues and briefly discusses the use of antihypertensive agents commonly administered in this setting.     

Determinants of stillbirth mortality in Greece

A population-based case-control study of the determinants of stillbirths was conducted in Greece from 1989 to 1991. All reported stillbirths after 28 weeks of pregnancy (N = 2,006) during the three year study period comprised the case group. The control group derived from random sampling of 10% of all livebirths in Greece, during the same period (N = 30,705). The data were analysed by modelling through multiple logistic regression. The adjusted relative risk of stillbirth was significantly higher for males compared to females. A statistically significant monotonic increase in relative risk was observed with shorter gestational age, low maternal education, and older maternal age. Birthweight and parity showed a statistically significant U-shaped association with stillbirth risk, with a higher risk being observed among both low and high birthweight deliveries, as well as among primiparous or multiparous (4+) mothers. Positive associations of stillbirth with multiple births, out-of-wedlock marriage and non-Greek-orthodox maternal religion were noted in crude analyses, but these associations almost disappeared in logistic regression model. Maternal urban or rural residence showed no relation to risk. Overall, the prospective risk of stillbirth after the 24th week of gestation in Greece has been estimated to be higher than that in Japan (a more developed country) with more than 40% of stillbirths occurring after the 36th week of pregnancy.     

Magnetic resonance imaging of intracerebral hemorrhage

Computerized tomography (CT) followed with magnetic resonance imaging (MRI) several years later enabled first the direct visualization of extravascular blood and products of it's degradation. Protein component of hemoglobin is from over 90% responsible for the hyperdensity of CT image in case of a hemorrhage, whereas paramagnetic properties of hemoglobin derivates are responsible for signal changes in MRI. CT is capable to diagnose accurately just an acute hemorrhage. It changes towards hypodensity in 3 weeks with posthemorrhagic pseudocyst as a final result that has rather low specificity. Differentiation from contusion, ischemic lesion or even astrocytoma may be difficult. CT has thus "short memory" for hemorrhage. MRI can differentiate 5 stages of hemorrhage according to the time schedule: hyperacute, acute, subacute stage I, subacute stage II and chronic. Sequel of a hemorrhage is detectable even years after the hemorrhagic event. The development of intracranial hemorrhage in daily routine MR imaging is described and documented to serve as a guide of model situation for the use of physician.     

The relationship of hospital ownership and teaching status to 30- and 180-day adjusted mortality rates

Hospital characteristics have been shown previously to be associated with variations in the probability of death within 30 days of admission. In the current study, the authors extend the examination of the relationship between hospital type to both short-term and long-term adjusted mortality. Observed and predicted 1988 hospital mortality rates were obtained from the Health Care Financing Administration (HCFA). A total of 3,782 acute care hospitals were divided into six mutually exclusive groups on the basis of their status as osteopathic, private for-profit, public teaching, public nonteaching, private teaching, and private nonteaching hospitals. After adjusting for the HCFA predicted mortality, Medicaid admissions, and emergency visits, 30-day and 30-to-180-day patient mortality rates were compared for these hospital types. Separate comparisons also were performed after stratifying hospitals into three groups defined by community size. The risk-adjusted 30-day mortality per 1,000 patients was 91.5, ranging from 85.4 for private teaching hospitals to 95.3 for nonteaching public hospitals, and 97.4 for osteopathic hospitals. The adjusted 30-to-180-day mortality was 84.7, ranging from 82.6 for nonteaching public hospitals to 87.4 and 88.2, respectively for public teaching and osteopathic hospitals. Differences among hospital types were minimal for small communities and increased with community size. In the large communities, the types of hospitals with high 30-day mortality also had higher mortality after 30 days. There was a strong association of hospital type with adjusted 30-day mortality, which should depend on the quality of hospital care, and a much weaker association with post-30-day mortality, which may be more dependent on patient risk. There was no evidence that types of hospitals with low 30-day mortality were postponing rather than preventing mortality.     

Determinants of the neonatal mortality

A recent sharp decline in the neonatal mortality in our medical center prompted a critical analysis of viral statistics of the newborn service during the years 1966 through 1973. The mean neonatal mortality for the entire period was 15.4 per 1,000 live births, and 11.0 in the period 1972 through 1973. The annual neonatal mortalities bore a direct relationship to the annual incidences of infants with birth weights of 1,500 gm or less. The reduction in the proportion of infants in the latter weight group during 1972 through 1973 accounted for three quarters of the improvement in the neonatal mortality as compared to that of the previous years. One quarter of the improvement could be attributable to a decrease in mortality that occurred only in infants in the latter weight group during the same period.     

Recurrence of bleeding in patients with hypertensive intracerebral hemorrhage

To characterize the recurrence of bleeding in patients who had hypertensive intracerebral hemorrhage (HICH), the authors reviewed 989 patients who underwent treatment for HICH between 1989 and 1995. Fifty-three patients (5.4%) had two episodes of HICH within a median interval of 22.9 +/- 16.3 months (range 1.5-72 months), and of these 3 (5.7%) had three episodes of HICH. The recurrence of bleeding most commonly occurred within 2 years of the first hemorrhage: in 66% of the 53 patients the second hemorrhage occurred soon after the first (within 1 year in 34%, within 1-2 years in 32.1%). The site of the second hemorrhage was different from the initial site in all patients. Only 1 patient had a third hemorrhage in the same site as the second hemorrhage. The common patterns of recurrence were 'ganglionic (putamen/caudate nucleus)-thalamic' in 26.8% and 'ganglionic-ganglionic' in 21.4%. The 'lobar-lobar' pattern was noted in only 2 patients. The volume of the hematoma was increased at the second hemorrhage. The overall mortality was 28.3%. The risk of recurrent hemorrhage significantly increased in the patients who had antihypertensive therapy of less than 3 months after the initial attack compared to those with further long-term therapy (p < 0.005). Long-term regular control for hypertension is needed to prevent recurrent hemorrhage.     

Predisposing factors to enlargement of spontaneous intracerebral hematoma

BACKGROUND AND PURPOSE: Enlargement of intracerebral hemorrhage is a major cause of clinical deterioration. Identification of factors that predispose to hematoma enlargement is important in managing patients. METHODS: We selected 186 patients (71 women and 115 men; mean age, 64.8 +/- 12.5 years) with spontaneous intracerebral hemorrhage who had undergone an initial CT within 24 hours and a second scan within 120 hours of symptom onset. We compared patients with (n = 41) and without (n = 145) hematoma enlargement according to clinical characteristics and laboratory data. RESULTS: By multiple logistic regression analysis (n = 139), interaction of long interval (> 6 hours) from onset to first CT and small hematoma (< 25 cm3) strongly reduced risk of enlargement. The analysis also demonstrated that the following factors independently predisposed to enlargement: history of brain infarction; liver disease; interaction of fasting plasma glucose > or = 141 mg/dL and systolic blood pressure on admission > or = 200 mm Hg; and interaction of glycosylated hemoglobin A1c > or = 5.1% and systolic blood pressure on admission > or = 200 mm Hg. CONCLUSIONS: A patient examined > 6 hours after ictus who has a hematoma volume < 25 cm3 is unlikely to experience further hematoma growth. Prevention of brain infarction and premorbid management of liver disease may serve to lower the risk of hematoma enlargement. Although it remains controversial whether antihypertensive drugs should be used in the acute phase of intracerebral hemorrhage, poorly controlled diabetics with high systolic blood pressure (> or = 200 mm Hg) on admission also were at high risk of hematoma enlargement.     

Metalloproteinase inhibition blocks edema in intracerebral hemorrhage in the rat

Clinical worsening often occurs 1 to 2 days after an intracerebral hemorrhage. Extracellular matrix proteolysis by metalloproteinases, which attack the basal lamina and open the blood-brain barrier, may be one contributing factor. Matrix metalloproteinases and plasminogen activators are increased 16 to 24 hours after a bacterial collagenase-induced intracerebral hemorrhage, suggesting that agents that block metalloproteinases may reduce the brain swelling after hemorrhage. Therefore, we injected 0.2, 0.3, 0.4, or 0.5 units bacterial collagenase intracerebrally in rats to produce an intracerebral hemorrhage. Twenty-four hours later, brain tissue was removed for measurement of brain water and electrolytes. Proteases were assayed by zymography. Treatment with a matrix metalloproteinase inhibitor, BB-1101, was begun 6 hours after the collagenase lesion, when the hematomas were formed and the secondary edema was increasing. Bacterial collagenase caused a dose-dependent hematoma at the injection site with secondary brain edema in both posterior regions. The lower bacterial collagenase doses (0.2 and 0.3 units) mainly caused brain edema in the tissue around the injection site, whereas the higher doses (0.4 and 0.5 units) also affected the opposite hemisphere. Administration of BB-1101 significantly reduced the brain water and sodium contents in regions away from the injection site in rats with 0.4 unit lesions (p < 0.05). Zymography showed an increase in 92-kDa type IV collagenase and urokinase-type plasminogen activator at 24 hours. Inhibitors of proteolytic cascade enzymes may be useful in treatment of secondary brain edema in intracerebral hemorrhage.     

Clinical aspects and diagnostic characteristics of nontraumatic intracerebral hemorrhage

The results of treatment of 235 young and middle age patients with nontraumatic intracerebral haemorrhage were analyzed. Diagnosis was verified with the help of computer tomography, magnetic-resonance tomography, angiography and basing on operational and autopsy data as well. Three main symptoms, reflecting the dislocational changes dynamics, were assigned.     

立体定向血肿清除术治疗中度高血压脑出血38例分析

目的:研究评价中度高血压脑出血立体定向血肿清除术的疗效.方法:将符合入组条件的高血压脑出血患者随机分成2组,手术组38例,保守治疗组40例,进行对照分析.结果:微创组的疗效优于保守组,差异具有显著性(P＜0.01).结论:中度高血压脑出血采用立体定向血肿清除术治疗的疗效明显优于单纯保守治疗.     

No evidence for an ischemic penumbra in massive experimental intracerebral hemorrhage

OBJECTIVES: To determine the effect of massive intracerebral hemorrhage (ICH) on regional cerebral blood flow (rCBF) and metabolism, and to test the hypothesis that there is persistent ischemia in the perihematoma region after ICH. BACKGROUND: Cerebral ischemia is postulated to be one of the mechanisms of neural injury after ICH. Presumably the hematoma induces ischemia by mechanical compression of the surrounding microvasculature. METHODS: The authors induced ICH in eight anesthetized mongrel dogs by autologous blood injection (7.5 mL) under arterial pressure in the deep white matter adjacent to the left basal ganglia. They measured serial rCBF using radiolabeled microspheres in regions around and distant to the hematoma, as well as cerebral oxygen extraction, oxygen consumption (CMRO2), glucose utilization, and lactate production by serial sampling of cerebral venous blood from the sagittal sinus. Mean arterial pressure (MAP) and intracranial pressure (ICP) were monitored continuously. All measurements were recorded at 0.5, 1.0, 2.0, 3.5, and 5.0 hours after induction of ICH and compared with prehematoma values. Evans Blue dye was injected at the end of the experiment, and intensity of staining was compared with three control animals. RESULTS: Compared with prehematoma ICP (12.5+/-2.0 mm Hg, mean+/-standard error), significant elevation in ICP was observed after ICH peaking at 5 hours (34.4+/-5.2 mm Hg). Compared with prehematoma MAP (125.8+/-7.0 mm Hg), significant elevation in MAP was observed at 120 minutes after onset of hematoma (139.1+/-4.6 mm Hg), with return to the prehematoma value by 5 hours. There were no significant changes observed in cerebral oxygen extraction (51.4+/-4.3% versus 44.8+/-4.9%) and CMRO2 (1.8+/-0.3 versus 1.64+/-0.2 mL O2/100 g/min) at 5 hours posthematoma (or any other posthematoma measurement) compared with prehematoma values. There were no significant differences observed in rCBF in the perihematoma gray (18.2+/-0.9 mL/100 g/min versus 20.1+/-1.5 mL/100 g/min) or white matter (15.6+/-1.4 mL/100 g/min versus 15.3+/-1.1 mL/100 g/min) at 5 hours posthematoma (or any other posthematoma measurement) compared with prehematoma values. No changes were observed in cerebral glucose utilization, lactate production, and rCBF in other regions after introduction of ICH. Permeability of the blood-brain barrier was more prominent in the ipsilateral hemisphere in animals with ICH compared with control animals. CONCLUSIONS: Despite a prominent increase in ICP and MAP after ICH, the authors found no evidence to support the presence of an ischemic penumbra in the first 5 hours after ICH. Thus, other mechanisms for acute neural injury and late rCBF changes after ICH must be investigated.     

Value of repeat angiography in patients with spontaneous subcortical hemorrhage

BACKGROUND and PURPOSE: Neuroradiological investigations do not disclose a source of bleeding in some patients with spontaneous subcortical hemorrhage. These patients may harbor undetected vascular malformations and may be at risk of rebleeding in the future. We investigated patients with subcortical hemorrhage with use of repeat angiography and MRI to determine the incidence of occult vascular malformations and the risk of bleeding during follow-up. METHODS: We reviewed a consecutive series of 137 patients with subcortical hemorrhage during a 10-year period (June 1987 through June 1997). If the patient was <65 years old and the first angiogram and/or MRI did not show a source of bleeding, repeat angiography was recommended. All angiographic and MRI studies were reviewed. The relationship between the identified bleeding source and clinical variables such as patient age, sex, and history of hypertension and the size and location of the hematoma were examined. RESULTS: One hundred seven patients (78%) underwent angiography on admission, 10 (7%) had immediate surgery for hematoma without angiography, and 20 (15%) had neither angiography nor surgery. Overall, an etiology for the hemorrhage was found in 55 cases (40%). Vascular malformations were common in young patients without preexisting hypertension. A second angiogram was obtained in 22 patients, and 4 arteriovenous malformations were demonstrated. Rebleeding at the site of the initial hemorrhage was not observed after a mean follow-up of 68 months. CONCLUSIONS: Angiography performed acutely after hemorrhage may not demonstrate vascular malformations. Consideration should be given to repeat angiography in patients who do not have a specific cause for hemorrhage.