[Vitreous hemorrhage after intracranial hemorrhage: Terson's syndrome].
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Eye↗
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Results for “Intracranial Hemorrhages”
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White-centered retinal hemorrhages: a sign of intracranial hemorrhage.
White-centered retinal hemorrhages (so-called "Roth spots") were seen in an 11-year-old girl with spontaneous intraventricular and subarachnoid hemorrhage from a ruptured "berry" aneurysm without underlying systemic disorder.
Cerebral Hemorrhage↗
Rapid detection of neonatal intracranial hemorrhage by transillumination.
Using transillumination and a sensitive cadmium sulfide light meter, 145 newborns were screened for the presence of intracranial hemorrhage. Intracranial hemorrhage (ICH) was suspected when the light meter could not detect any light passing through the anterior fontanel when the light beam was directed through the frontal eminence. ICH was confirmed by branial computed tomography or postmortem examination in all 17 infants not transmitting light. Spectrophotometry was performed on samples of cerebrospinal fluid (CSF) to demonstrate the mechanism through which blood in the CSF blocks light transmission.
Cadmium↗
[Computed tomographic findings in intracranial hemorrhage due to ruptured intracranial aneurysm (author's transl)].
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Adult↗
Computerized tomography in intracranial hemorrhage.
Three hundred patients with intracranial hemorrhage were studied by computerized tomography (CT). Thalamic-ganglionic hematoma was found in 232; the mortality increased from 25% to 70% if ventricular extension occurred in this group. Lobar hematoma occurred in 45 of these patients, with a mortality of 20%, which was not influenced by ventricular extension. Seven had intraventricular bleeding only; of these, two died. In 12 patients with CT evidence of cisternal blood, angiography demonstrated aneurysms; the location of the blood predicted the location of the aneurysm in six. Multiple spontaneous intracerebral hematomas (ICHs) were visualized by CT in five patients. In 29 of 146 cases of ICH, postcontrast study showed enhancement; in 15, this was consistent with neoplasm, angioma, or aneurysm. In 14 with spontaneous ICH, ring enhancement occurred ten days to six weeks following hemorrhage.
Adult↗
Four autopsy cases of neonatal giant cell hepatitis died suddenly and unexpectedly from intracranial hemorrhage.
The authors present four cases of neonatal giant cell hepatitis who died suddenly and unexpectedly from intracranial hemorrhage, autopsied recently at the Tokyo-to Medical Examiner Office. This series consisted of one male and 3 female infants ranging from 37 to 52 days of age. The cause of death of all cases was thought to be massive intracranial hemorrhage. Referring to the connection between intracranial hemorrhage and neonatal giant cell hepatitis, it was assumed that the former must have occurred due to the hemorrhagic tendencies of the latter, superimposing to the hemorrhage at birth trauma of the head. As to the formation of multinucleated giant cell, it is considered to be of degenerative nature of hepatocytes, i.e. the giant cell is formed by fusion of hepatocytes as a result of the disappearance of bile canaliculi, although the etiology of this hepatitis is still unknown.
Brain↗
Changes in clinical presentation of term infants with intracranial hemorrhage.
The clinical course and outcome of eight term infants with intracranial hemorrhage are reported. Before computerized tomography became available, term infants with intracranial hemorrhage were usually diagnosed only at autopsy and the hemorrhage was associated with a trauamtic birth or severe asphyxia. In contrast, since the availability of computerized tomography, term infants with a diagnosis of intracranial hemorrhave have a non-traumatic delivery, present with seizures, and survive.
Cerebral Hemorrhage↗
[Timing of a letal intracranial hemorrhage by means of the HbA/HbF ratio (author's transl)].
Possibilities and limits of the method for timing an intracranial hemorrhage by means of the HbA/HbF erythrocyte ratio are investigated in six newborns. The effect of labeling HbF erythrocyte containing newborn blood by transfusion and exchange transfusion of HbA erythrocyte containing donor blood as well as "self-labeling" after the first transfusion as a result of HbA--and HbF erythrocytes decaying at a different rate, is described. If a coagulum can be clearly allocated to the blood where it originates from, depends a) on the alteration of the HbA/HbF erythrocyte ratio by the above mentioned ways of labeling and b) on the size of the sample i.e. on the number of erythrocytes counted to determine the HbA/HbF erythrocyte ratio. The confidence limits of the HbA/HbF erythrocyte ratio for a given number of counted erythrocytes have been determined. It was taken into account whether the blood was labelled by a transfusion or by "self-labeling". The analysis of the period before, during and after the intracranial hemorrhage made a preliminary evaluation of etiological factors and some symptoms possible. The hypothesis that sodium bicarbonate dosages of 8 mEqu/kg/24 h are an important cause of intracranial hemorrhage has to be rejected on the grounds of this study's results.
Cerebral Hemorrhage↗
The influence of route of delivery and hyaline membranes on the risk of neonatal intracranial hemorrhages.
The relationship of route of delivery and hyaline membranes to eight sites of intracranial hemorrhage was evaluated in 513 autopsied newborn infants. Those delivered by cesarian section appeared to be at less risk for most hemorrhages compared with newborns delivered vaginally. However, the reductions in risk were small and did not achieve nominal levels of statistical significance. Thus, "birth trauma" probably contributes little to the risk of most neonatal intracranial hemorrhages. Newborns who developed hyaline membranes appeared to be at greater risk for most hemorrhages than those who did not, particularly if the infant had been delivered by cesarian section. This was especially marked for subarachnoid and germinal matrix hemorrhage.
Cerebral Hemorrhage↗
Hypoglycorrhachia in neonatal intracranial hemorrhage. Relationship to posthemorrhagic hydrocephalus.
The level of cerebrospinal fluid (CSF) glucose may be lowered after subarachnoid hemorrhage. This was observed in each of 18 cases of proven posthemorrhagic hydrocephalus in infants (study group). In one of these children with a hemorrhagic spinal fluid and hypoglycorrhachia unaccompanied by clinical signs of intracranial hemorrhage or hydrocephalus, the axial tomography showed a significant although asymptomatic hydrocephalus. To further evaluate the significance of this finding (hypoglycorrhachia), we compared the incidence of hypoglycorrhachia (CSF glucose less than 40 mg) and lowered CSF glucose/blood glucose ratio (ratio less than 0.4) at three similar time intervals from the presumed time of the intracranial hemorrhage in the study group with that of a control group of 40 neonates with similar neonatal associated pathology (mainly premature infants with hyaline membrane disease) but who did not later develop posthemorrhagic hydrocephalus or cerebral palsy. There was a statistically greater frequency of these anomalies in the hydrocephalic group. Only 3 of the 40 control patients had hypoglycorrhachia and low ratio. Hypoglycorrhachia in the absence of other known causes for decreased CSF glucose is a good index of a probably significant meningeal hemorrhage with a high risk of secondary hydrocephalus which may or may not be symptomatic. Hypoglycorrhachia may be used as an indication of the frequency of clinically inapparent subarachnoid hemorrhage in these high risk newborns.
Cerebrospinal Fluid Proteins↗
Intracranial hemorrhage and infarction in anticoagulated patients with prosthetic heart valves.
In 1 year 6 patients with prosthetic heart valves (PHVs) treated with anticoagulants suffered intracranial hemorrhage. In 4, hemorrhage occurred into the site of a recent non-hemorrhagic infarction. In the others, both of whom had endocarditis, hemorrhages probably occurred as the result of rupture of a mycotic aneurysm. Five patients were treated with warfarin, 1 with heparin. In all patients the level of anticoagulant activity was greater than 1.5 times control. Five patients were in atrial fibrillation; 1 was hypertensive. The diagnosis of intracranial hemorrhage was made and its location and extent accurately determined by computed tomography (CT). Three patients underwent surgery and 2 are alive with only minor neurological deficits. Among the 3 patients who did not undergo surgery 2 died and 1 is alive with a moderate neurological deficit. The management of PHV patients with use of anticoagulants is discussed in terms of the mechanisms involved in intracranial bleeding. Emphasis is placed on prevention of emboli, discontinuation of anticoagulants once non-hemorrhagic infarction has occurred and the primacy of CT scan in diagnosis when hemorrhage is suspected. The special problems of anticoagulation in the presence of endocarditis are also discussed.
Aged↗
CT detection and course of intracranial hemorrhage in premature infants.
Twenty neonates with a suspected intracranial hemorrhage were studied by computed tomography (CT). The exact site and extent of the hemorrhage in all infants were clearly demonstrated on serial CT scans. In intraventricular hemorrhage, a dense subependymal halo lined the ventricular system and could be recognized for up to 2 weeks. Discrete hemorrhage adjacent to the ventricular system also appeared as discrete nodules rather than as a diffuse hemorrhage. Blood in the ventricular system could be recognized up to 2 weeks when there were blood-cerebrospinal fluid levels. Hydrocephalus was a common sequela and was readily detectable before a measurable change in head size.
Cerebral Hemorrhage↗
Blood pressure management after endovascular thrombectomy in acute ischemic stroke: association with symptomatic intracranial hemorrhage and functional outcome at 3 months.
BACKGROUND: No clear consensus exists on ideal systolic blood pressure (SBP) targets after endovascular thrombectomy (EVT) following an acute ischemic stroke (AIS). This study investigated the association between SBP parameters within the first 24 h after EVT and 3-month functional outcomes and the risk of symptomatic intracranial hemorrhage (sICH). METHODS: We retrospectively collected and prospectively followed clinical, and radiological data for patients undergoing EVT for AIS from 2016 to 2024, including 2-hourly BP measurements during the first 24 h and SBP variability assessed by standard deviation (SD) and coefficient of variation (CV). Outcomes included 3-month functional status and sICH, and their associations with post-EVT BP metrics were analyzed. RESULTS: A total of 268 post EVT patients were included with a median age of 61 years (IQR, 51-69). Mean SBP was 129.67 ± 17.17 mm Hg, with SBP variability (SD 12.6 ± 5.4 mm Hg; CV 9.6 ± 3.8 %), while good functional outcome and sICH occurred in 39.7 % and 4.9 % of patients, respectively. Multivariate regression showed that higher admission NIHSS (>15) [0.90 (95 %CI, [0.86, 0.95], p = 0.000)], recanalization status [1.88 (95 %CI, [1.43, 2.48], p = 0.00)], and SBP-CV ≥ 10 [0.44 (95 %CI, [0.2, 0.94], p = 0.036)] was independently associated with poor 3-month functional outcome, while higher admission NIHSS (>15) [0.87 (95 %CI, [0.77,0.98], p = 0.02)] and diabetes [0.12 (95 %CI, [0.03, 0.54], p = 0.006)] predicted increased risk of sICH. CONCLUSIONS: The study showed that reduced BP variability during the first 24 h post-EVT was associated with better 3-month functional outcomes. A clear association between SBP and sICH risk was not demonstrated.
Humans↗
[Neuropathological study of adult intracranial hemorrhage. General data in 500 cases].
The systematic pathological study of 500 patients with intracranial hemorrhages (ICH) [341 (68 P. 100) CEREBRAL HEMORRHAGES (C.H.); 119 (24 p. 100) meningeal hemorrhages (M.H.); 39 (7,8 p. 100) subdural hematomas (S.H.) and, at last, one extradural hematoma] has been practiced. Those cases were issued primarily from neurological and, at a lesser degree, from neurosurgical departments. Etiological data, complications, associated findings and causes of death have been analysed. High blood pressure is the main etiological factor in C.H. This is confirmed by the statistical comparison between the incidence of this factor in our material and in the whole French population. However, nearly 50 p. 100 of ICH occuring in normotensive patients are C.H. The incidence of cirrhosis is much higher in our study than in other reports from the literature. The frequently associated high blood pressure does not seem to enhance the incidence of CH in patients with liver cirrhosis. Although this last factor can be found alone, its real etiological importance in CH cannot be assessed on account of the lack of data concerning the incidence of liver cirrhosis in the French population. The incidence of anticoagulant therapy is high in S.H. On the contrary, this factor does not seem to enhance the risk of high blood pressure induced C.H. The traumatic etiology of S.H. is significantly higher than the anticoagulant therapy etiology which, however, is very high in our study.
Adult↗
Concentration of 3', 5' cyclic adenosine monophosphate in ventricular cerebrospinal fluid of patients with prolonged coma after head trauma or intracranial hemorrhage.
A previous study showed that cerebrospinal fluid from the lateral ventricle of patients without disturbance of sensorium or intracranial pressure contains 15 to 30 nm 3', 5' cyclic adenosine monophosphate. We measured the concentration of this cyclic nucleotide by radioimmunoassay in cerebrospinal fluid from the lateral ventricle of six patients with prolonged coma (20 days or longer) after head trauma (four), or spontaneous intracranial hemorrhage (two). Coma was graded IV to I in order of decreasing severity. Fluid was removed at intervals of six to 72 hours from a Rickham reservoir placed in the lateral ventricle. Concentration of the cyclic nucleotide (mean +/- S.E.M.) in coma of Grades IV, III, II and I was 2.1 +/- 0.3, 4.6 +/- 0.5, 6.3 +/- 1.4 and 12.5 +/- 2.4 nM respectively. After sensorium became normal, cAMP was 21.0 +/- 1.4 nM. Correlation between grade of coma and concentration was -0.89 (P less than 0.01). Thus, prolonged coma appears to be associated with a disturbance of cyclic AMP metabolism within the central nervous system.
Adult↗
Pulmonary edema following intracranial hemorrhage.
Hemodynamic changes and samples of fluid from pulmonary edema were studied in a 50-year-old woman who developed florid pulmonary edema following intracranial hemorrhage. Marked systemic and pulmonary arterial hypertension were associated with the rapid production of edema fluid that contained red blood cells, but had a lower protein content than plasma. After restoration of pulmonary vascular pressures to a normal range, the production of fluid ceased, and clinical signs of edema resolved. These findings point to the sudden increase in pulmonary microvascular pressure as the cause of pulmonary edema in this patient. Our findings contrast with those of previous reports and with speculations on the extent of a defect in permeability accounting for pulmonary edema following injury to the brain.
Albumins↗
Evaluation of neonatal intracranial hemorrhage by computerized tomography.
Computerized tomographic (CT) brain scan was performed on 28 infants with unexplained cardiorespiratory and neurologic deterioration and bloody lumbar cerebrospinal spinal fluid. Fourteen of 20 with intraventricular hemorrhage (IVH) died; the six infants with lesser degrees of IVH survived. Significant subarachnoid hemorrhage (SAH) was demonstrable in three infants and three had negative scans despite bloody CSF. We have found that CT scans provide useful information about the size and extent of neonatal IVH and distinguished it from SAH. It also confirms the diagnosis of post-hemorrhagic hydrocephalus in these infants. Continued use of the CT scan will help us to understand the natural history and the effects of neonatal intracranial hemorrhage among the survivors of intensive care.
Cerebral Hemorrhage↗
[Intracranial hemorrhage in autopsy cases with occlusion of the circle of Willis (author's transl)].
Seventeen autopsy cases with occlusion of the circle of Willis were examined clinicopathologically. These patients ranged in age from 8 years to 64 years and consisted of 6 males and 11 females. The following results were obtained. 1. Fresh and massive intracerebral hemorrhage was confirmed in 13 of 17 patients and cerebral infarct in 4 of 17 patients. 2. Among these 13 patients, massive hemorrhage was found in basal ganglia, thalamus and hypothalamus of 9 patients, and in thalamus, cerebral peduncle and midbrain of 4 patients. 3. Rupture of the dilated muscular-type arteries was noted in the thalamus and basal ganglia in 2 of 13 patients. Ruptured arteries with organization of the lumen were found in the old hemorrhagic foci in one of them. 4. Overgrown and dilated arteries, branching off from the circle of Willis, were confirmed in 11 patients. These arteries consisted of "perforating" arteries well developed as collateral circulation. 5. No ruture in these arteries of the subarachnoidal spaces was found in 11 patients. In one of them, a small saccular aneurysm was found. These findings strongly suggest that in patients with occlusion of the circle of Willis intracerebral rupture of overgrown "perforating" arteries as collateral circulation may be the main cause of intracranial hemorrhage and intracerebral hemorrhage due to rupture of the arteries may be repeated.
Adolescent↗