The pathogenesis of some cases of cerebral hemorrhage (a morphologic study of thmargins of hemorrhagic foci and areas of the brain distant form the hemorrhage).
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
It has been reported that the reduction of cerebral blood flow (CBF) is more pronounced with thalamic hemorrhages than with putaminal hemorrhages, and the clinical outcome is worse with the former. However, the mechanism underlying these differences is not clear. We compared neurologic status, hematoma volumes, outcome scores. and early (< 1 month) and late (2-12 month) CBF values between 15 patients with thalamic hemorrhages and 28 patients with putaminal hemorrhages. We also correlated thalamic versus hemispheric CBF on each side and ipsilateral versus contralateral thalamic and hemispheric CBF. Finally, we evaluated the response to acetazolamide during the late stage. Thalamic hemorrhages were associated with a more pronounced reduction in CBF bilaterally, even though their hematoma volumes were much smaller. Contralateral to the hemorrhage, the discrepancy in CBF values between the two groups became greater in the late stage because CBF started to recover in putaminal hemorrhages but persistently deteriorated in thalamic hemorrhages. In the group with thalamic hemorrhages, the correlation between thalamic and hemispheric CBF ipsilateral to the hemorrhage and between thalamic CBF on both sides was disrupted in the early stage and restored in the late stage, whereas the correlation between the hemispheric CBF values was consistently preserved. Acetazolamide invariably augumented CBF during the late stage. The clinical outcome was worse in the thalamic group, but CBF values correlated negatively with outcome in both groups. We conclude that the reduction of CBF in the late stage may be secondary to metabolic depression due to transneural depression ('diaschisis'). The metabolic depression in thalamic hemorrhages is more extensive and persistent than in putaminal hemorrhages, which probably accounts for both the more pronounced CBF reduction and the worse outcome.
OBJECTIVE: To report the visual and anatomic outcome after surgical drainage of suprachoroidal hemorrhage according to hemorrhage severity. DESIGN: A retrospective chart review. PARTICIPANTS: Forty-eight consecutive eyes undergoing surgical drainage of a suprachoroidal hemorrhage at The Medical College of Wisconsin were examined. INTERVENTION: Demographic and clinical data were abstracted from patients' medical records. Eyes were classified into four categories of increasing hemorrhage complexity: (1) nonappositional choroidal hemorrhage without vitreous or retinal incarceration in the wound (12 eyes); (2) centrally appositional choroidal hemorrhage without vitreous or retinal incarceration in the wound (17 eyes); (3) choroidal hemorrhage with associated vitreous incarceration in the wound (11 eyes); and (4) choroidal hemorrhage with associated retinal incarceration in the wound (8 eyes). MAIN OUTCOME MEASURES: Visual acuity, rate of persistent hypotony, and incidence of irreparable retinal detachment after surgical drainage for four classes of suprachoroidal hemorrhage were defined. RESULTS: Overall, 11 (23%) of 48 eyes had no light perception (NLP) vision develop, 9 (19%) of 48 eyes had persistent postsurgical hypotony (intraocular pressure < 6), and 21 (64%) of 33 eyes with retinal detachment enjoyed successful retinal reattachment surgery. A definite trend toward an increased rate of NLP vision (P < 0.02), persistent hypotony (P < 0.05), and irreparable retinal detachment (P = 0.11) was observed with increasing suprachoroidal hemorrhage complexity. Eyes with retinal incarceration, compared to eyes without retinal incarceration, had an increased rate of NLP vision (63% vs. 15%; P < 0.01), persistent postsurgical hypotony (50% vs. 13%; P < 0.05), and irreparable retinal detachment (50% vs. 20%; P = 0.07). CONCLUSIONS: Eyes requiring surgical drainage of a suprachoroidal hemorrhage have a guarded prognosis, with a poorer outcome associated with increasing hemorrhage complexity. A classification system incorporating choroidal apposition, and vitreous and retinal incarceration in the wound, provides a format for reporting and assessing the efficacy of management strategies in this condition.
The pathogenesis of hemorrhage induced by three purified components of rattlesnake (Crotalus atrox) venom was studied at the light and electron microscopic levels. Crude venom was fractionated by anion exchange and gel filtration in four steps. beta-Alanine acetate disk gel electrophoresis was used to demonstrate electrophoretic homogeneity. White mice were injected intramuscularly with 0.1 ml of a sublethal dose of hemorrhagic toxin. Gross examination revealed extensive hemorrhage 5 minutes after the injection of hemorrhagic toxins alpha and episilon; the same amount of hemorrhage was not present until 3 hours after the injection of hemorrhagic toxin beta. Light microscopic examination of muscel after injection of the toxins revealed areas of extensive hemorrhage in which very few intact capillaries could be found and also adjacent areas of slight hemorrhage in which capillaries were in various stages of degeneration. Necrosis of muscle cells was evident in tissue injected with hemorrhagic toxin beta. Electron microscopic examination showed that capillaries from toxin-injected muscle were in various stages of degeneration. Endothelial cells became very thin and broke down into vesicles prior to complete rupture. Gaps were formed within the cells while intercellular junctions remained intact. Plasma and erythrocytes leaked through these gaps and were observed in the endomysium. Many gaps were plugged with platelet aggregations. Collagen and the basal lamina associated with capillaries were usually disorganized or absent. The experimental injection of three purified hemorrhagic toxins induced hemorrhage by the same mechanism as does the crude venom, ie, per rhexis. In addition, one of the toxins, hemorrhagic toxin beta, causes myonecrosis.
PURPOSE: To investigate the sequential changes in heart rate (HR), autonomic nervous activity presented by the spectral analysis of heart rate variability (HRV), hemodynamics and metabolism during massive hemorrhage and progressive hemorrhagic shock in dogs. METHODS: Twelve dogs were subjected to acute massive hemorrhage until mean arterial pressure (MAP) reached 50 mm Hg. Then bleeding was stopped and they were allowed to reach a plateau phase. They were divided, post hoc, into bradycardic or tachycardic groups according to their HR response to the acute massive hemorrhage. After reaching a plateau phase, the dogs were further bled to keep their MAP around 50 mmHg (progressive hemorrhagic shock). Their heart rate power spectra were quantified into low-frequency (LF) (0.04-0.15 Hz) and high-frequency (HF) (0.15-0.4 Hz) components. RESULTS: In the bradycardic group, both LF and HF increased after massive hemorrhage, but during progressive hemorrhagic shock these components decreased while HR increased. In the tachycardic group, LF increased after massive hemorrhage, but during progressive hemorrhagic shock LF decreased with continuous suppression of HF CONCLUSION: Massive hemorrhage caused two types of HR response: bradycardia and tachycardia. The HRV profile showed differential autonomic characteristics, and could be a valuable tool in assessing various degrees of hemorrhagic shock.
Trehalose dimycolate (TDM) is a glycolipid contained in the cell walls of Mycobacteria, Nocardia and Corynebacteria. An intraperitoneal injection of TDM into mice has been known to produce hemorrhagic pneumonia without affecting any other organs. Thus, it provides a unique experimental model for studies of the mechanisms of alveolar hemorrhagic syndrome, including idiopathic pulmonary hemosiderosis. It has been reported that T lymphocytes are essential for the production of TDM-induced hemorrhagic pneumonia, however, the overall cellular mechanism is not yet clear. The purpose of this study is to re-examine and clarify the role of T lymphocytes in the pathogenesis of TDM-induced hemorrhagic pneumonia. To achieve it we considered 1) the dynamics of infiltrating lymphocytes to find out if there is a certain T lymphocyte subpopulation infiltrating predominantly into the lung, 2) the effect of in vivo depletion of T lymphocyte subpopulation by monoclonal antibodies, and 3) the effect of transfer of T lymphocytes into nude mice. The analysis of the dynamic change of the number of lymphocytes showed that the number of L3T4+ cells as well as Lyt2+ cells decreased on day 2 or 3 after TDM injection, thereafter increased, however, neither subpopulation infiltrated predominantly into the lung. Alveolar hemorrhages occurred in L3T4+ cell-depleted and/or Lyt2+ cell-depleted mice, and hemorrhages were enhanced in Lyt2+ cell-deplete mice. Alveolar hemorrhages occurred even in nude mice, and the intensity of hemorrhages or the cell numbers in the lung did not differ from those in T lymphocyte-reconstituted nude mice, however, hemorrhages were enhanced in L3T4+ cell-reconstituted nude mice. These results suggested that T lymphocytes are not primarily involved in the cellular mechanisms of the pathogenesis of TDM-induced hemorrhagic pneumonia, however, L3T4+ cells modify the process of the production of hemorrhagic pneumonia secondarily and enhance it.
Five previously unknown hemorrhagic proteins, designated hemorrhagic toxins a,b,c,d, and e, were isolated from the venom of the western diamondback rattlesnake (Crotalus atrox). Molecular weights of hemorrhagic toxins a-e were determined to be 68 000, 24 000, 24 000, 24 000, and 25 700, respectively, by sodium dodecyl sulfate-phosphate gel electrophoresis using various polyacrylamide gel concentrations. Amino acid composition showed a total of 636, 200, 213, 214, and 219 amino acids for hemorrhagic toxins a-e, respectively. All the hemorrhagic toxins were found to lose their hemorrhagic activities with the metal chelators ethylenediaminetetraacetic acid and 1, 10-phenanthroline. All the hemorrhagic toxins were found to contain approximately 1 mol of zinc/mol of toxin, and they were all demonstrated to be proteolytic when dimethylcasein and dimethylhemoglobin were used as substrates. When zinc was removed from hemorrhagic toxin e with 1,10-phenanthroline, both both the proteolytic and hemorrhagic activities were equally inhibited. When the apohemorrhagic toxin e thus produced was incubated with zinc, the hemorrhagic and proteolytic activities were regenerated to the same extent. CD, UV, and Raman spectroscopy were used to study the structure of native hemorrhagin toxin e as well as the structural changes caused by zinc removal. From CD spectroscopy the native toxin was estimated to consist of 23% alpha helix, 6% beta structure, and 71% random-coil conformation. When over 90% of the zinc was removed, the alpha-helix content dropped from 23 to 7%.
PURPOSE: To investigate the correlation between a disc hemorrhage and peripapillary atrophy in glaucoma patients with a unilateral disc hemorrhage. METHODS: The 44 glaucoma patients (7 with primary open-angle glaucoma and 37 with normal-tension glaucoma) with a unilateral disc hemorrhage from June 1997 to November 2002 were selected randomly and included sequentially. The topographic measurements were performed using Heidelberg Retina Tomograph (HRT) within 3 months of detecting the disc hemorrhage. The zone beta parameters of the peripapillary atrophy were analyzed by the Atrophy Zone Analysis software. The intraocular pressure, refractive error, visual field parameters, and optic disc parameters were compared between both eyes. Univariate and multivariate regression analysis were performed. RESULTS: The area, angular and radial extent of the zone beta, and the ratio of the zone beta area to the disc area were significantly greater in the hemorrhagic eyes than in the contralateral eyes (P < 0.001). The prevalence of peripapillary atrophy was significantly higher in the hemorrhagic eyes (84%) than in the contralateral eyes (66%) (P = 0.034, chi2 test). The rim area and the rim volume of the hemorrhagic eyes were significantly smaller than those of the contralateral eyes (P = 0.02, < 0.001, respectively). In multivariate regression analysis, the peripapillary atrophy area was the independent significant factor associated with disc hemorrhage (P = 0.03, Odds Ratio = 1.51). The refractive error, intraocular pressure, Mean Deviation (MD), and Corrected Pattern Standard Deviation (CPSD) of the visual fields in both eyes were similar. CONCLUSION: The area and extent of the peripapillary atrophy was significantly greater and more prevalent in the eyes with a disc hemorrhage than in the contralateral control eyes. Peripapillary atrophy is closely associated with a disc hemorrhage in glaucoma patients irrespective of small neuroretinal rim area and volume.
OBJECTIVE: The aim of this community-based study was to investigate the incidence rates and outcome of primary intracerebral hemorrhage (ICH) in relation to the site of hemorrhage. METHODS: The subjects were 350 patients with primary first-ever ICH who were treated during the 8-year period 1991 to 1998 in Izumo City, Japan. RESULTS: The crude and age- and sex-adjusted incidence rates for all types of ICH were 52 and 47 per 100,000 population, respectively, for all ages. The most common site of ICH was the putamen (120 patients, 34%), followed by the thalamus (115, 33%), lobar areas (53, 15%), brainstem (30, 9%), cerebellum (25, 7%), and caudate nucleus (7, 2%). The crude and age- and sex-adjusted annual incidence rates per 100,000 population were 18 and 16 for putaminal, 17 and 15 for thalamic, 8 and 7 for lobar, 4 and 3 for cerebellar, 4 and 4 for brainstem, and 1 and 1 for caudate hemorrhages, respectively. The Glasgow Coma Scale scores on admission were best in patients with cerebellar hemorrhage and worst in those with brainstem hemorrhage. Surgery was performed for 34% of putaminal, 9% of thalamic, 14% of caudate, 21% of lobar, and 32% of cerebellar hemorrhages but not for brainstem hemorrhages. The 30-day case fatality rate was 11% for putaminal, 9% for thalamic, 14% for caudate, 11% for lobar, 0% for cerebellar, and 53% for brainstem hemorrhages. When patients with ICH were analyzed as a whole, the overall survival rates at 30 days, 3 months, and 3 years were 87, 83, and 73%, respectively. Both the short-term and long-term outcomes after ICH were directly related to the site of hemorrhage and the severity of bleeding, which was assessed by the hematoma volume and Glasgow Coma Scale score. Overall, 190 (54%) of 350 patients had a favorable outcome, and 55 (16%) had died at discharge. CONCLUSION: Marked differences were observed in the incidence rates and outcome of primary ICH in relation to the site of hemorrhage. The differences in outcome were primarily a result of differences in the severity of bleeding for each ICH subtype.
Although most previous reports recommended operative treatments for ovarian hemorrhages, management of idiopathic ovarian hemorrhage with massive intraabdominal hemorrhage has not been established yet. In order to evaluate effectiveness of non-operative management for idiopathic ovarian hemorrhage, 3 patients with idiopathic ovarian hemorrhage and massive intraabdominal hemorrhage (700-1,400 ml) were managed conservatively and monitored by ultrasonography. Non-operative management had successful results in two of the three patients and the other case showed a spontaneous hemostasis of ovarian bleeding at operation. As the first therapy for idiopathic ovarian hemorrhage without any severe complications, non-operative management should be chosen to avoid pelvic adhesions. 700-1,000 ml of intraabdominal hemorrhage were found to be naturally absorbed in a week by ultrasonography. This is the first to report that natural absorption of massive intraabdominal hemorrhage associated with idiopathic ovarian hemorrhage was captured in details by ultrasonography.
PURPOSE: To describe the clinical features and to present results of new diagnostic methods to help define the cause of the clinical syndrome of intrapapillary hemorrhage with adjacent peripapillary subretinal hemorrhage (IHAPSH). DESIGN: Retrospective review of patients with IHAPSH at presentation seen in 3 centers in Hawaii and Japan. METHODS: We analyzed data including patient demographics, presenting symptoms, initial and final visual acuities, biomicroscopic findings, fundus photographs, and results of available ancillary testing, including fluorescein angiography, B-scan ultrasonography, and optical coherence tomography. RESULTS: There were 10 eyes of 9 patients (7 female and 2 male, 8 Asian and 1 white) aged 14 to 79 years. All patients experienced an acute onset of visual symptoms. Eight eyes had mild to severe myopia (-2.50 diopters [D] to -9.50 D), and 8 eyes had a tilted disc. Hemorrhage within the disc and adjacent subretinal hemorrhage were located nasally in 6 eyes, superiorly in 2 eyes, and temporally in 2 eyes. Vitreous hemorrhage was noted in 6 of 10 eyes. Posterior vitreous evaluation by biomicroscopy (10 eyes), by B-scan ultrasonography (4 eyes), and by optical coherence tomography (2 eyes) revealed no evidence of vitreopapillary traction, except for a follow-up optical coherence tomography in 1 eye showing localized vitreoretinal separation with residual attachment to the optic disc 10 months after presentation. Fluorescein angiography showed mild disc staining in 4 of 8 eyes. Hemorrhage spontaneously resolved within 1 to 7 months, and there were no recurrent hemorrhages with an average follow-up of 13.5 months (range, 2-31 months). Visual acuities maintained or improved to 20/25 or better in 8 eyes. The other 2 eyes had unrelated poor vision. CONCLUSIONS: Intrapapillary hemorrhage with adjacent peripapillary subretinal hemorrhage is more common in myopic eyes and spontaneously resolves without treatment. The unique structural architecture of the elevated nasal edge of the myopic tilted disc and the choroidal blood supply of the prelaminar optic nerve may predispose patients to bleeding from the optic discs, which may be spontaneous or may be precipitated by acute disc edema, Valsalva maneuver, or vitreopapillary traction.
A retrospective study of 320 patients with spontaneous subarachnoid hemorrhage revealed a 20.8% incidence of intraocular hemorrhages. While diagnostically helpful, intraocular hemorrhages also were prognostically significant. The overall patient mortality was 31.6%. In those with intraocular hemorrhages the mortality was 53.6% compared to 19.7% in those without intraocular hemorrhages. Fifty-eight percent with bilateral intraocular hemorrhages died versus 48% with unilateral hemorrhages. Vitreous hemorrhage, though infrequent, may be a major complication in survivors of subarachnoid hemorrhage.
Intracerebral contusions can lead to regional ischemia caused by extensive release of excitotoxic aminoacids leading to increased cytotoxic brain edema and raised intracranial pressure. rCBF measurements might provide further information about the risk of ischemia within and around contusions. Therefore, the aim of the presented study was to compare the intra- and perilesional rCBF of hemorrhagic, non-hemorrhagic and mixed intracerebral contusions. In 44 patients, 60 stable Xenon-enhanced CT CBF-studies were performed (EtCO2 30 +/- 4 mmHg SD), initially 29 hours (39 studies) and subsequent 95 hours after injury (21 studies). All lesions were classified according to localization and lesion type using CT/MRI scans. The rCBF was calculated within and 1-cm adjacent to each lesion in CT-isodens brain. The rCBF within all contusions (n = 100) of 29 +/- 11 ml/100 g/min was significantly lower (p < 0.0001, Mann-Whitney U) compared to perilesional rCBF of 44 +/- 12 ml/100 g/min and intra/perilesional correlation was 0.4 (p < 0.0005). Hemorrhagic contusions showed an intra/perilesional rCBF of 31 +/- 11/44 +/- 13 ml/100 g/min (p < 0.005), non-hemorrhagic contusions 35 +/- 13/46 +/- 10 ml/100 g/min (p < 0.01). rCBF in mixed contusions (25 +/- 9/44 +/- 12 ml/100 g/min, p < 0.0001) was significantly lower compared to hemorrhagic and non-hemorrhagic contusions (p < 0.02). Intracontusional rCBF is significantly reduced to 29 +/- 11 ml/100 g/min but reduced below ischemic levels of 18 ml/100 g/min in only 16% of all contusions. Perilesional CBF in CT normal appearing brain closed to contusions is not critically reduced. Further differentiation of contusions demonstrates significantly lower rCBF in mixed contusions (defined by both hyper- and hypodense areas in the CT-scan) compared to hemorrhagic and non-hemorrhagic contusions. Mixed contusions may evolve from hemorrhagic contusions with secondary increased perilesional cytotoxic brain edema leading to reduced cerebral blood flow and altered brain metabolism. Therefore, the treatment of ICP might be individually modified by the measurement of intra- and pericontusional cerebral blood.
The effects on the vascular system of a purified toxin, hemorrhagic proteinase IV, from Crotalus horridus horridus venom were studied with emphasis on the pathogenesis of hemorrhage. White mice were injected intramuscularly with sublethal doses of the hemorrhagic toxin, and tissue samples were obtained at 5 and 30 min, 3 and 24 hr after the injection. There was a good correlation between amount of toxin injected and amount of hemorrhage. Microscopically, extensive areas of hemorrhage around muscle and adipose cells were observed just 5 min after injection. At later time periods the changes were similar, but the hemorrhage was more extensive. Many vessels were plugged by aggregations of platelets. Electron microscopy showed that endothelial cells of capillaries were affected to various degrees. Some were swollen and had plasma membranes that formed large blebs; others were thin and disrupted. In vessels where the intercellular junctions could be observed, they were intact even when the endothelial cells were damaged or ruptured, indicating hemorrhage per rhexis instead of per diapedesis. Basal lamina were often disorganized or absent. Both intravascular and extravascular fibrin deposition were commonly observed. Hemorrhagic proteinase IV from C. h. horridus venom induces hemorrhage per rhexis and platelet aggregation within 5 min of intramuscular injection into mice, and marked fibrin deposition within 30 min of injection.
Clinically encountered hemorrhagic shock is usually caused by a single, rapid hemorrhage secondary to trauma. Experimental models of shock, however, have utilized anesthetic agents and hemorrhage protocols which may compromise the clinical relevance of their findings. This report characterizes the response of conscious, splenectomized dogs to a single hemorrhage of varying rates and volumes, uncomplicated by the presence of anesthetic agents. The duration of a 40 ml kg-1 hemorrhage affected the magnitude of blood pressure recovery, but did not alter the decompensating drop in blood pressure. The shortest hemorrhage duration was chosen for further study, as the blood pressure profile for this hemorrhage duration demonstrated most clearly the recovery, plateau, and decompensation phases. Increasing the hemorrhage volume to 43 ml kg-1 caused a reproducible decrease in the magnitude of the blood pressure recovery, the time to decompensation, and the time to death. Splenectomized dogs, then, demonstrate a reproducible response to a fixed-volume hemorrhage, making chronically instrumented conscious dogs a good animal model with which to study the progression of hypovolemic shock.
BACKGROUND: Hemorrhage is commonly treated with intravenous infusion of crystalloids. However, the dynamics of fluid shifts between body fluid spaces are not completely known, causing contradictory recommendations regarding timing and volume of fluid infusions. The authors have developed a turnover model that characterizes these fluid shifts. METHODS: Conscious, chronically instrumented sheep (n = 12) were randomly assigned to three protocol groups: infusion of 25 ml/kg of 0.9% saline over 20 min (infusion only), hemorrhage of 300 ml (7.8 +/- 1.1 ml/kg) over 5 min (hemorrhage only), and hemorrhage of 300 ml over 5 min followed by infusion as noted above (hemorrhage plus infusion). A two-compartment volume turnover kinetic model containing seven model parameters was fitted to data obtained by repeated sampling of hemoglobin concentration and urinary excretion. RESULTS: The volume turnover model successfully predicted fluid shifts. Mean baseline volumes of the central and tissue compartments were 1799 +/- 1276 ml and 7653 +/- 5478 ml, respectively. Immediate fluid infusion failed to prevent hemorrhage-induced depression of cardiac output and diuresis. The model suggested that volume recruitment to the central compartment after hemorrhage was primarily achieved by mechanisms other than volume equilibration between the two model compartments. CONCLUSION: Volume turnover kinetics is a promising tool for explaining fluid shifts between body compartments after perturbations such as hemorrhage and intravenous fluid infusions. The pronounced inhibition of renal output after hemorrhage prevailed regardless of fluid infusion and caused fluid retention, which expanded the tissue compartment.
OBJECTIVE: To determine the occurrence of upper gastrointestinal hemorrhage in critically ill children, and the efficacy of prophylaxis with almagate (antacid), ranitidine, and sucralfate. DESIGN: Prospective, randomized, controlled trial. SETTING: Pediatric ICU of a tertiary care pediatric hospital. PATIENTS: During a 2-yr study period, 165 patients with one or more upper gastrointestinal hemorrhage risk factors were randomized into one of four groups. Twenty-five patients were excluded because of protocol violations. A total of 140 patients completed the study, with 35 patients in each group. INTERVENTIONS: Patients received no treatment in the control group. The antacid group received almagate 0.25 to 0.5 mL/kg every 2 hrs by nasogastric tube. The ranitidine group received 1.5 mg/kg every 6 hrs iv. The sucralfate group received 0.5 to 1 g every 6 hrs by nasogastric tube. METHODS: Gastric pH and macroscopic bleeding were determined every 2 hrs in all patients until the end of the study. Macroscopic bleeding was classified as nonhemorrhage, slight, or important. Microscopic gastric bleeding was researched with guaiac testing in 72 patients (680 samples). The severity of illness was evaluated by using the Therapeutic Intervention Scoring System, Physiologic Stability Index, and the Multiorgan System Failure scores. The risk of upper gastrointestinal hemorrhage was evaluated by the Zinner and Tryba indices, and was modified for children. MEASUREMENTS AND MAIN RESULTS: The occurrence rate of important upper gastrointestinal hemorrhage was higher (by 20%) in the control group than in the rest of the groups (5.7%), p less than .01. There were no differences between the other groups (almagate 5.7%, ranitidine 8.5%, and sucralfate 2.8%). There was a statistically significant correlation between the occurrence rate of important upper gastrointestinal hemorrhage, the scores of severity of illness indices (Therapeutic Intervention Scoring System, Physiologic Stability Index, and the Multiorgan System Failure scoring system), the risk of upper gastrointestinal hemorrhage indices (Zinner and Tryba), and mortality rate. The Zinner index better classified the patients in relation to the onset of important upper gastrointestinal hemorrhage (sensitivity 76.9%, specificity 85.8%). CONCLUSIONS: Upper gastrointestinal hemorrhage is an important complication in critically ill children. Prophylaxis with almagate, ranitidine, or sucralfate reduces the occurrence rate of clinically important gastrointestinal hemorrhage.
BACKGROUND AND PURPOSE: Assessment of possible hemorrhage in acute stroke before appropriate therapy remains important. The aim of this study was to determine the frequency with which patients present with clinical stroke and have intracranial hemorrhage on initial noncontrast head CT scan (NCCT). In addition, we sought to determine the frequency with which initial clinical diagnosis acute stroke is confirmed in this group. METHODS: Medical records of 691 consecutive patients with admitting diagnosis of acute stroke were evaluated retrospectively. Results of initial NCCT performed within 24 hours after presentation were assessed. All patients were examined before anticoagulation or thrombolysis. Correlation with treatment and leading differential etiology was made. RESULTS: Twenty-five patients (25/691 [3.6%]) had hemorrhage. Twenty-three patients (23/25 [92%]) had intraparenchymal hemorrhage only. One patient (1/25 [4%]) had a combination of intraparenchymal and subarachnoid hemorrhage. One patient (1/25 [4%]) had subdural hemorrhage only. Twenty-two NCCT scans (22/25 [88%]) were performed within 6 hours of presentation. Seventeen NCCT scans (17/25 [68%]) were performed within 3 hours of presentation. CONCLUSION: Despite frequent concerns for intracranial hemorrhage complicating acute stroke and treatment, a low percentage of patients had this complication. Moreover, our frequency is much lower than the wide ranges reported elsewhere. The most common type of intracranial hemorrhage in this cohort was intraparenchymal, but subarachnoid and subdural hemorrhages were also diagnosed and must also be considered. Twenty-eight percent of patients with initial suspicion of acute ischemic stroke are eventually given other diagnoses. These results may have implications for use of CT imaging.