[Pathophysiology of brain edema--general remarks].
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Animals↗
Biomedical subjects
U Ito
Publications and source records attributed to U Ito.
High colloid oncotic therapy for contusional brain edema.
We investigated whether prolonged high colloid oncotic therapy for two weeks can suppress contusional brain edema. Eighteen patients with cerebral contusion were randomly divided into two groups of patients receiving high oncotic pressure (HOP; 26-30 mmHg) treatment and those receiving normal oncotic pressure (NOP; 22-26 mmHg) treatment. Oncotic pressure was maintained for two weeks with administration of a 25% albumin solution with additional use of furosemide. Edema volume was calculated by summation of all measured low-density areas in each CT slice multiplied by 1.0 cm of slice of thickness. We expressed contusional brain edema volume as a percent increase based on each patient's initial CT. The mean percent increase of contusional brain edema in the NOP group was significantly higher than that in the HOP group at 9-15 days (208.9% and 14.0%, respectively) and 16-25 days (188.8% and 10.0%, respectively). There were no complications such as heart failure or renal failure during treatment. All the patients in the HOP group recovered with minimal or no neurological deficit. On the other hand, 30% of patients in the NOP group remained in poor condition. With frequent measurement of oncotic pressure and adjustment of fluids and electrolytes, continuous oncotic therapy for two weeks effectively and safely reduced contusional brain edema.
Adolescent↗
Chronological changes in brain edema induced by experimental intracerebral hematoma in cats.
To investigate the temporary profile of changing perifocal brain edema around an intracerebral hematoma (ICH), we developed an experimental ICH model using cats. The developing perifocal edema in the white matter around the hematoma was measured by means of a gravimetric technique. Edema was more severe near the ICH, and declined with increasing distance. Edema was mild 2 hours after the onset of the ICH, and was most severe in all the regions examined 3 days later. Edema decreased but still existed in all regions 7 days after the onset of the ICH. The results suggest that the mechanism of the development of edema associated with ICH seems to differ from that associated with a cold injury. This experimental ICH model proved to be useful for the study of formation, expansion, and resolution of edema associated with ICH.
Animals↗
High colloid oncotic therapy for brain edema with cerebral hemorrhage.
We examined the effectiveness of high colloid oncotic pressure (COP) therapy to suppress and/or reduce brain edema associated with putaminal hemorrhage of patients whose clinical grades were grade 3 or 4a classified according to the Japanese neurological grading for putaminal hemorrhage. In the treated group of 11 patients, 25% albumin solution was intravenously administered (50-100 ml/day) with additional use of furosemide (20-40 mg/day) following hematoma removal. The serum COP was maintained at 25-30 mmHg for 2 weeks. In the untreated group of 11 patients, the COP therapy was not applied following hematoma removal. The serum COP was 20-25 mmHg for 2 weeks thereafter. During the 2-week observation period, serum osmolality, electrolyte, and hematocrit levels did not significantly differ between the two groups. The midline structure shift on CT of the treated group was 4.5 mm, which was significantly smaller than that of the untreated group (p < 0.05). The numbers of patients either in the vegetative state or death were 0 and 3, respectively, in the treated and the untreated groups. We concluded that high COP therapy for 2 weeks following hematoma removal was effective to suppress and/or reduce brain edema associated with putaminal hemorrhage, and that this therapy could be continued for 2 weeks without systemic complications.
Adult↗
Effect of acetazolamide on early ischemic cerebral edema in gerbils.
Acetazolamide was given in the early stage of ischemic cerebral edema produced by unilateral permanent carotid occlusion in gerbils. The animals were studied 1, 4, and 6 hours after ischemia. The tissues were examined for water and electrolyte concentrations and ischemic areas were visualized by 2,3,5-triphenyltetrazolium chloride (TTC) and H-E staining. Acetazolamide injected just after occlusion showed a positive effect in reducing edematous changes. Later administration of the drug had neither positive nor harmful effect on the ischemic brains. Thus, acetazolamide seems to be useful for cerebrovascular response studies in the early stage of a brain lesion.
Acetazolamide↗
Peritumoral edema in meningioma: a contrast enhanced CT study.
The propagation of extravasated contrast medium around 6 supratentorial meningiomas with peritumoral white matter of low density (PWL) of Lanksch II-III was investigated by repeated CT scanning at 4 h intervals, following a 1 h drip infusion of 200 ml of Iopamidol. The volume of the expanding peritumoral contrast enhancement was calculated according to a method previously described. By calculating the increase in volume from the first to the second scan, and from the second to third, we derived the rate of edema formation as well as the resolution rate of edema in the PWL. The surface area of the entire tumor (TS) and area of tumor surface facing the PWL (LS) were calculated by summating the surface areas of all CT slices, each area of which was derived from the measured length of the entire circumference of the tumor and circumference of the tumor facing the PWL, respectively, multiplied by the slice thickness of 0.5 cm. The volume of PWL, edema formation rate of entire tumor, and tumor volume x LS/TS were well correlated with each other. We concluded that the severity of peritumoral edema in meningiomas depends on the size of the tumor and the extent of tumor surface contact with the PWL.
Aged↗
Atrophy and maldevelopment of the ipsilateral cerebral hemisphere after acute subdural hematoma in infants.
Among nine infants aged less than 4 years with acute subdural hematoma admitted between 1980 and 1991, five required evacuation of a hematoma. Eight of them survived longer than 1 month and the remaining patient who had a hematoma removal died 3 days postoperatively. The four infants who required evacuation of a hematoma and survived longer than 1 month had prolonged hemispheric swelling ipsilateral to the hematoma lasting for 2 weeks postoperatively. Intracranial pressure was higher than 25 mm Hg during this period. Diffuse high density was observed in the affected hemisphere in one patient 12 days after injury, which was assumed to be hemorrhagic infarction. Subsequently, these four infants developed atrophy of the cerebral hemisphere ipsilateral to the hematoma. The pathophysiology of the atrophy of the cerebral hemisphere ipsilateral to the acute subdural hematoma is discussed.
Acute Disease↗
Repeated unilateral carotid occlusion in Mongolian gerbils: quantitative analysis of cortical neuronal loss.
To develop an experimental model which enables quantitative analysis of chronic neuronal loss in the cerebral cortex, repeated ischemic insult was performed using unilateral carotid artery occlusion in Mongolian gerbils. The effect of the time interval between the repeated ischemic insult on the survival rate of the animals and the amount of cortical neuronal loss were examined. The time course of the cortical neuronal damage in repeated ischemic insult was also studied. We repeated the occlusion four times; i.e., one 10-min and three 7-min occlusions (total 31 min of ischemia). The number of animals surviving for 3 weeks after the last ischemic insult was minimum (15.4%) for animals undergoing occlusions at 1-h intervals and maximum (100%) at 24- and 48-h intervals. The number of ischemic neuronal deaths was also dependent upon the time interval, and it was so pronounced as to allow analysis at intervals of 12 hr or 24 hr in the absence of infarction in the cortex. The number of neuronal deaths could not be determined for animals with occlusion at 1-h intervals due to the production of a large infarction, with which the 3-week survival rate was minimum. The temporal profile of cortical neuronal loss in the repeated ischemic insult at 24-h intervals indicated that the number of cortical neurons significantly decreased until 7 days after the start of the ischemic procedure. This model is useful for clarifying the pathophysiology of chronically developing ischemic neuronal death.
Animals↗
Changes in cranial and rectal temperature, blood pressure and arterial blood gas during and after unilateral and bilateral forebrain ischemia in Mongolian gerbils.
Transient forebrain ischemia was produced by occluding the common carotid arteries, either unilaterally or bilaterally, in Mongolian gerbils under halothane anesthesia. After 20-min ischemia, the cranial temperature measured in the temporal muscle decreased compared to the preischemic level, the decrease being larger after the bilateral than after the unilateral occlusion. After recirculation, cranial temperature recovered promptly to the preischemic level in the unilateral group, while it was elevated to above the preischemic level in the bilateral group. The rectal temperature also decreased with a similar time course. During 30-min ischemia, the blood pressure of both groups increased to above the preischemic level, the increase being larger in the bilateral group than in the unilateral group. After recirculation, blood pressure of the unilateral group recovered promptly to the preischemic level, while that of the bilateral group decreased to below the preischemic level. When forebrain ischemia was produced immediately after cessation of halothane inhalation, blood pH, PaO2 or PaCO2 did not change significantly from the control level. However, these values showed larger variation in the bilateral group than in the unilateral group. Unilateral occlusion in preselected gerbils provided a good model of transient brain ischemia, giving rise to uniform experimental results.
Animals↗
[Measurement of serum colloid oncotic pressure as a parameter of hemodilution and hemoconcentration in hypervolemic-hyperdynamic therapy for symptomatic vasospasm].
Nineteen patients, who developed symptomatic vasospasm due to subarachnoid hemorrhage, were treated by hypervolemic-hyperdynamic therapy. The object of this treatment was to increase cardiac output and cerebral blood flow as a result of hypervolemia and the administration of beta-stimulants. During the treatment, if cerebral infarction occurred followed by brain edema, we applied oncotic therapy. As the parameters of therapy, we measured serum colloid oncotic pressure and cardiac functions in all of these patients. Nineteen patients were divided into two groups: group A, 9 patients, who did not develop brain edema, and group B, 10 patients, who developed brain edema. All patients underwent acute neck clipping surgery and plasma volume expansion by the infusion of albumin and/or low molecular weight dextran (LMWD). If symptomatic vasospasm occurred, a Swan-Ganz catheter was inserted and cardiac output was measured until it increased to 1.5 times the value of pretreatment. In group B, we also used oncotic therapy, raising serum oncotic pressure higher than 25 mmHg by increasing the amount of albumin and/or LMWD and administering furosemide. By this treatment, the percentage of patients who showed neurological improvement in at least one deficit was 100% in group A, and 89% in group B. In Glasgow outcome scale scores, 89% of group A and 70% of group B had disability not lower than moderate. Serum colloid oncotic pressure was maintained at around 20-25mmHg in group A, and 25-30mmHg in group B. Although pulmonary artery diastolic pressure in group B tended to be lower than that in group A, cardiac indices in both groups were high, approximately 5.0 L/min/m2.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac Output↗
[Clinical features of main and peripheral pulmonary artery stenosis: significance of auscultation and phonocardiography].
Twenty-five patients with main and peripheral pulmonary artery stenosis were studied to determine the most frequently observed diagnostic sign of this abnormality regardless of the underlying etiologies, such as intrinsic or extrinsic narrowing of the pulmonary artery due to tumor, fibromuscular dysplasia, thromboembolism, angitis including the aortitis syndrome (Takayasu arteritis) and a variety of other disease entities. Among a variety of signs and symptoms, we emphasized the importance of cardiac auscultation and phonocardiography, which were often the initial diagnostic clues. The diagnostic features included a systolic murmur of pulmonary arterial origin and the behavior of the splitting of the second heart sound. The systolic murmur was often trans-systolic or continuous. In cases with left-sided cardiac murmurs (Takayasu arteritis, etc), the pulmonary systolic murmurs were not identified by auscultation alone and required phonocardiographic confirmation. In many cases the second heart sound was split and this was sometimes the first clue to the diagnosis. The split intervals varied, but were more marked in cases with pulmonary hypertension, and were accompanied by the accentuated pulmonic component (IIP). Phonocardiographic analysis disclosed that wide splitting was caused by the delayed appearance of IIP as well as the concomitant early appearance of the aortic component (IIA). It was concluded that, although the final etiological diagnosis is not identified, auscultation and phonocardiography provide important clues for further diagnostic and etiological studies of pulmonary artery stenosis.
Adolescent↗
Formation and resolution of white matter oedema in various types of brain tumours.
Following infusion of 200 ml of Iopamidol for 1 hour the propagation of extravasated contrast medium around different types of 12 brain tumours was examined and imaged via CT. Increasing volume of expanding peritumoural contrast enhanced brain tissue was measured by integrating volumes of planimetrically measured enhanced area on CT slice of 0.5 cm in thickness. So far our data failed to demonstrate differences in the peritumoural contrast expansion between the different types of tumours. Formation and resolution as well as the speed of oedema propagation were determined by calculation of the increasing volume of the enhanced peritumoural brain tissue. Average formation rate of oedema fluid from 1 cm3 of tumour was 0.06 ml/hr, and was lower in larger tumours, while formation rate of oedema fluid from whole tumour was higher in larger tumours. Average resolution rate of oedema fluid during the passage through 1 cm3 of the peritumoural white matter was 0.03 ml/hr, and was not affected by tumour size. Average speed of oedema propagation was 0.59 mm/hr, and was higher in larger tumours. The main therapeutic effect of steroid in peritumoural oedema was a reduction in formation rate of oedema fluid.
Brain Edema↗
Peritumoral brain edema. A keynote address.
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Adrenal Cortex Hormones↗
A computed tomography study on formation, propagation, and resolution of edema fluid in metastatic brain tumors.
Propagation of contrast medium, which extravasated from small metastatic brain tumor, was imaged via CT. By maintaining a constant blood level of the contrast medium by prolonged infusion of 200 ml of 60% meglumine amidtrizoate for 3 hr and thus maintaining a constant passage of contrast labeled edema fluid into the peritumoral extracellular space, the spread of the newly formed edema fluid can be imaged by repeated CTs as a gradually expanding peritumoral circular enhancement into the neighboring white matter. Four patients with small metastatic brain tumor were investigated. CT scans were taken at identical levels 1.5, 3, 6, 9, and 12 hr after start of contrast infusion. After 4 to 7 days of dexamethasone treatment (0.15-0.25 mg/kg/day), the examination was repeated. The area of the expanding circular enhancement was planimetrically measured. From these values, the increase in radius per hour, respectively, in volume per hour were calculated assuming a spherical geometry. These data enabled a determination of the formation rate of edema fluid, of the speed of edema propagation, and of the resolution rate of edema fluid during tissue passage. The formation rate of edema fluid amounted to 0.6 to 3.2 ml/hr depending on tumor diameter and was reduced by about 30% after dexamethasone treatment. Edema fluid traveled 4.8 mm during the first 180 min and 1.9 mm during the consecutive 90 min. The resolution rate of edema fluid during tissue passage amounted to 0.05 ml/hr/cm3 white matter before dexamethasone treatment.
Brain Edema↗
Cerebral atrophy after severe head injury.
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Adult↗
Formation and propagation of brain oedema fluid around human brain metastases. A CT Study.
Computerized tomography (CT) was used to examine the time-course of the propagation of extravasated contrast medium from small brain metastases into the peritumoural oedematous white matter, following infusion of 200 ml of meglumine amidtrizoate for 3 hours. Four patients with a metastatic brain tumour were examined. CT scans at identical levels were taken 1.5, 3, 6, 9, and 12 hours after start of contrast infusion. Following 4-7 days of dexamethasone treatment (8-12 mg/day i.v.) the examination was repeated. A contrast-enhanced area was observed surrounding the clearly delineated tumours, expanding gradually in a circular fashion into the peritumoural white matter oedema. The expanding circular enhancement was measured planimetrically on the various scans. From these values, the increase in radius/hr respectively in volume/hr was calculated, assuming a spherical geometry. This enabled a determination of the rate of oedema fluid formation and of the speed of oedema fluid propagation. The formation rate of oedema fluid amounted to 0.5-3.2 ml/hour and the speed of oedema fluid spreading to 1.9 mm/hour. Following treatment with dexamethasone the formation rate of oedema fluid is reduced by 30-50%. The important clinical implications of these new findings are discussed.
Aged↗
Factors affecting the extension of peritumoural brain oedema. A CT-study.
In human brain tumours the extension of peritumoural brain oedema may vary considerably. 37 brain tumours of various pathology and 2 abscesses were examined to identify the factors and mechanisms responsible for the oedema spreading. Peritumoural oedema profiles were determined towards the white matter and ventricle by measuring the CT-numbers of consecutive tissue blocks of 3.0-3.6 mm from the tumour to the normal white matter or the ventricle. It was found that neither the size of the tumour nor the histology has a close relationship to the amount of peritumoural oedema. The distance of oedema spreading rather is determined by the amount of fluid accumulation in the white matter immediately bordering the tumour. This relationship corresponds to a semilogarithmic function and represents the relation between the tumour-adjacent accumulation of extracellular fluid volume and the distance of extracellular fluid movement. The analysis of this relation leads to the suggestion that pressure gradients and bulk flow are involved in the development of human peritumoural oedema.
Brain Edema↗
[Ventriculo-peritoneal shunt malfunction with anti-siphon device in normal-pressure hydrocephalus. Report of three cases].
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Cerebral Ventriculography↗