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1 lial/endothelial cell dysfunction (edema and hemorrhage).
2 of significant subinternal limiting membrane hemorrhage).
3 ubarachnoid hemorrhage with intraventricular hemorrhage).
4 cluding patients diagnosed with subarachnoid hemorrhage).
5  in ischemic stroke and 42% in intracerebral hemorrhage.
6 ral microbleeds (CMBs) as a marker of occult hemorrhage.
7 and treatment of the underlying mechanism of hemorrhage.
8 d with long-term outcome after intracerebral hemorrhage.
9 less, CNS blood vessels were intact, without hemorrhage.
10      LFL was observed as an evolving retinal hemorrhage.
11 ents, 88 lobar, and 40 deep intraparenchymal hemorrhage.
12 ssociated hemolysis, or after a subarachnoid hemorrhage.
13 olar wall rupture may be sufficient to cause hemorrhage.
14 odalities for treatment of diabetic vitreous hemorrhage.
15 age in patients with aneurysmal subarachnoid hemorrhage.
16 are patients with hypofibrinogenemia-induced hemorrhage.
17 by 2 months of age primarily due to internal hemorrhage.
18 ar blood vessels that often lead to cerebral hemorrhage.
19 dence in the initial evaluation of suspected hemorrhage.
20 or pre-retinal hemorrhage, and mild vitreous hemorrhage.
21 schemic stroke, and 2,974 with intracerebral hemorrhage.
22 IVA was given with complete clearance of the hemorrhage.
23 ularizations elsewhere (NVEs) and preretinal hemorrhage.
24 icted poor outcome in lobar intraparenchymal hemorrhage.
25 gow Outcome Scale) in lobar intraparenchymal hemorrhage.
26 es, and 4% (95% CI, 0.01-0.1%) intracerebral hemorrhage.
27 t be assessed in patients with intracerebral hemorrhage.
28  are common vascular anomalies causing brain hemorrhage.
29 ing 53 with sepsis and 59 with intracerebral hemorrhage.
30 hospitalization for bleeding or intracranial hemorrhage.
31 hance associations with disease severity and hemorrhage.
32 sculature, which result in aneurysms and eye hemorrhages.
33 Twelve of the RCNs were active with exudates/hemorrhages.
34 nocytes was found in 39 (93%) white-centered hemorrhages.
35 patients with thick versus thin subarachnoid hemorrhage (1.92 vs 1.99 mg/dL; p = 0.022).
36 ied Fisher scale (grades: 0, no radiographic hemorrhage; 1, thin [< 1 mm in depth] subarachnoid hemor
37 of gastrointestinal bleeding or intracranial hemorrhage (12.9 per 1000 person-years) compared with th
38 7]; P = .29), or progression of intracranial hemorrhage (16% vs 20%; difference, -5.4% [95% CI, -12.8
39 hage; 1, thin [< 1 mm in depth] subarachnoid hemorrhage; 2, thin subarachnoid hemorrhage with intrave
40                                 Subarachnoid hemorrhage (20%) was the most common type of intracrania
41               Within 1 year of intracerebral hemorrhage, 224 (56%) of 402 patients died.
42 brain injury (44%), followed by intracranial hemorrhage (24%), and ischemic infarct (16%).
43 ; P = 0.003), higher proportion with macular hemorrhage (25.5% vs. 13.2%; P = 0.014), and fewer anti-
44 atitis (PEP) (16.1% vs. 6.4%, p = 0.17), and hemorrhage (3.2% vs. 8.5%, p = 0.35).
45 (1.1%), ischemic stroke (1.9%), intracranial hemorrhage (3.5%), and brain death (1.6%).
46 ubarachnoid hemorrhage with intraventricular hemorrhage; 3, thick [>= 1 mm] subarachnoid hemorrhage;
47 , subretinal hemorrhage (51%), and choroidal hemorrhage (30%).
48  intracerebral hemorrhage (8%), and subdural hemorrhage (4%).
49  hemorrhage; 3, thick [>= 1 mm] subarachnoid hemorrhage; 4, thick subarachnoid hemorrhage with intrav
50 auma (62%), lens expulsion (54%), subretinal hemorrhage (51%), and choroidal hemorrhage (30%).
51          In contrast, rates of intracerebral hemorrhage (6% vs 8%; p = 0.35) did not differ.
52 -5.6% to 11.0%]) or symptomatic intracranial hemorrhage (7 [4.7%] vs 2 [1.3%]; unadjusted risk differ
53 unadjusted risk for symptomatic intracranial hemorrhage (7.7% versus 4.8%) and in-hospital mortality
54 patients [100%] vs 12 of 17 patients without hemorrhage [71%], P = .01) and development of the acute
55 ranial hemorrhage, followed by intracerebral hemorrhage (8%), and subdural hemorrhage (4%).
56 .9% vs 30.6%, P = 0.400), postpancreatectomy hemorrhage (9.1% vs 5.1%, P = 0.352), delayed gastric em
57 le performing vitrectomy for severe vitreous hemorrhage, a point of strong adherence between a old he
58  intracranial aneurysm leads to subarachnoid hemorrhage, a severe type of stroke.
59 table/potentially preventable (P/PP) deaths, hemorrhage accounted for 55.1%.
60 sed probability of symptomatic intracerebral hemorrhage (adjusted OR per 30 minutes increase in time
61 y perfusion and reduced intestinal edema and hemorrhage after BD.
62  subhyaloid, outer plexiform, and subretinal hemorrhages after 2 minutes of chest compressions.
63  of a retinal tear, pre-retinal and vitreous hemorrhages after completing a session of whole-body vib
64 eatic fistula, bile leak, postpancreatectomy hemorrhage (all ISGPS grade B/C), severe complications (
65 ing 53 with sepsis and 59 with intracerebral hemorrhage, along with 53 control participants.
66 tricular tachycardia, upper gastrointestinal hemorrhage, anaphylactic reaction, acute kidney injury,
67  between asymptomatic neonates with subdural hemorrhage and control neonates.
68            Ripk3 deficiency reduces cerebral hemorrhage and delays the onset of neural damage mediate
69  with the occurrence of side effects such as hemorrhage and edema.
70 of hepatic decompensation (ascites, variceal hemorrhage and hepatic encephalopathy), which defines th
71                              TIC exacerbates hemorrhage and is associated with higher morbidity and m
72 ment of all-cause mortality of intracerebral hemorrhage and ischemic stroke patients admitted to the
73         Patients with lobar intraparenchymal hemorrhage and lateralized rhythmic delta activity were
74 ly activates necroptosis to promote cerebral hemorrhage and neuroinflammation.
75 e, a point of strong adherence between a old hemorrhage and retinal surface was identified and manage
76 y nets, increasing the risk of intracerebral hemorrhage and stroke.
77                  At month 6, the presence of hemorrhage and the change in central subfield thickness
78 ied risks of serious side effects, including hemorrhages and cerebrospinal fluid leakage.
79 ression to PDR including the surface area of hemorrhages and the distance of hemorrhages from the ONH
80 g 10 with sepsis and five with intracerebral hemorrhage, and 11 healthy controls.
81 n imaging findings such as ischemic infarct, hemorrhage, and acute hemorrhagic necrotizing encephalop
82  (95% CI = 59-457%) in risk of intracerebral hemorrhage, and an increase in white matter hyperintensi
83 AS), increases the risk of preterm delivery, hemorrhage, and death.
84 greater infarct expansion, increased cardiac hemorrhage, and delayed neutrophil accumulation, which r
85 d inflammation resolution, increased cardiac hemorrhage, and enhanced cardiac dysfunction.
86 tter, indirect hyperbilirubinaemia, cerebral hemorrhage, and mental status change (in two [12%] patie
87  temporal retinal tear, inferior pre-retinal hemorrhage, and mild vitreous hemorrhage.
88 daptive immunity, coagulation abnormalities, hemorrhage, and multiorgan failure with up to 33% case f
89 on and fundus photography were evaluated for hemorrhage, and spectral-domain (SD) OCT images from HAR
90  dilated and sclerotic segments, perivenular hemorrhages, and foci of phlebitis.
91 inding, reduced VE-cad levels, microvascular hemorrhaging, and decreased survival.
92 normal blood cells, predisposing patients to hemorrhage, anemia, and infections.
93                     There was no evidence of hemorrhage, anemia, or AVMs in major organs to explain t
94 We conclude that the rates of thrombosis and hemorrhage appear to be similar following hospital disch
95 al extension, and a large proportion of such hemorrhages are likely to be a result of mechanisms othe
96 na, consistent with the finding that retinal hemorrhages are often found in multiple layers of the re
97  disorders (thrombocytopenia, thrombosis and hemorrhage) are risk factors for SARS-CoV-2-associated m
98 tinopathy in the multivariate model included hemorrhage area (odds ratio [OR], 2.63; 95% confidence i
99 aphy session, we classified intraparenchymal hemorrhage as isolated deep (no insular, subarachnoid, s
100 mon phenomenon after aneurysmal subarachnoid hemorrhage (aSAH) and contributes to neurocognitive decl
101 ents with high-grade aneurysmal subarachnoid hemorrhage (aSAH) is only insufficiently displayed by cu
102 sis differed between aneurysmal subarachnoid hemorrhage (aSAH) patients with surgical clipping and en
103                   In aneurysmal subarachnoid hemorrhage (aSAH), accurate diagnosis of aneurysm is ess
104  dreaded sequelae of aneurysmal subarachnoid hemorrhage (aSAH), requiring timely intervention with th
105 ter Acute Stroke Due to Spontaneous Cerebral Hemorrhage Associated With Antiplatelet Therapy trial, o
106  perfusion and reducing intestinal edema and hemorrhage associated with BD.
107 m revealed tortuous veins and a flame shaped hemorrhage at 7 o'clock.
108 ble analyses identified presence of vitreous hemorrhage at baseline, increasing age, absence of epire
109 1.9, 14.2); bevacizumab-treated eyes without hemorrhage at month 6 had a mean VALS improvement of 3.2
110  follow-up, aflibercept-treated eyes without hemorrhage at month 6 had a mean VALS improvement of 8.0
111 I: -4.6, 11.0); and observation eyes without hemorrhage at month 8 had a mean VALS improvement of 13.
112 mHg; 95% CI, 1.02-1.12; P = 0.008), and disc hemorrhage at visit 1 (HR, 2.08; 95% CI, 1.07-4.04; P =
113 t study eyes (89% [973/1095]) showed macular hemorrhages at baseline, declining to 31% (319/1042) at
114 pillary alterations; however, intra-alveolar hemorrhages, bacterial deposition, and markers of coagul
115 ge >15 years of age with evidence of truncal hemorrhage below the diaphragm and decision for emergent
116 lts diagnosed with spontaneous intracerebral hemorrhage between June 1, 2010 and May 31, 2013.
117 ative pancreatic fistula, postpancreatectomy hemorrhage, bile leakage, delayed gastric emptying, woun
118       Delirium is common after intracerebral hemorrhage, but severe neurologic deficits may confound
119                              Reduced area of hemorrhage by month 6 was observed in 70.7% (116 of 164)
120 nticoagulants were a factor in 3 retrobulbar hemorrhage cases.
121 lusion criteria included other intracerebral hemorrhage causes, anticoagulation, coagulopathy, or imm
122  content, fibrous cap structure, intraplaque hemorrhage), complementing the clinical lesion classific
123 ration before transfer and 34.9% experienced hemorrhage complications.
124 he CT scan, to identify retinal and vitreous hemorrhages consistent with TS.
125 elow the diaphragm and decision for emergent hemorrhage control intervention within 60 minutes of arr
126 a novel strategy to obtain earlier temporary hemorrhage control, supporting cardiac, and cerebral per
127      In 75, REBOA was utilized for temporary hemorrhage control.
128 proved diagnostic performance for predicting hemorrhage-control interventions and mortality compared
129 owing BOP by assessing the extent of surface hemorrhage/contusion, Hematoxylin and Eosin staining, an
130  demonstrated ~ 8.5 psi is the threshold for hemorrhage/contusion, up to 30 exposures.
131 ely collected at different time-points after hemorrhage: days 0-1 (acute); days 2-4 (pre-VSP); days 5
132 ome, in part by reducing BSCB disruption and hemorrhage decreasing cytotoxic neuroinflammation and at
133 indings that would bias toward PPV (vitreous hemorrhage, dense cataract, proliferative vitreoretinopa
134 The origin of blood in glaucoma-related disc hemorrhages (DH) remains unknown.
135 l 47 to 53 consists of 3 main features: deep hemorrhages (DH), venous beading (VB), and intraretinal
136 old girl with bilateral multilayered retinal hemorrhages due to SBS.
137                               Improvement in hemorrhage during follow-up was associated with visual a
138                        Relative to eyes with hemorrhage during follow-up, aflibercept-treated eyes wi
139 s (modified Fisher Scale (mFS), Subarachnoid Hemorrhage Early Brain Edema Score) (P < 0.05).
140 al hemorrhage (sICH), and major extracranial hemorrhage (ECH) within 90 days.
141  with both ischemic stroke and intracerebral hemorrhage, especially compared with other populations o
142 ive Surgery Plus Alteplase for Intracerebral Hemorrhage Evacuation Phase III trial.
143 strain caused high mortality, intra-alveolar hemorrhages, extensive alveolar septal sequestration of
144            Greater tumor thickness, vitreous hemorrhage, exudative retinal detachment, and poor basel
145  diagnostic brain CT for acute intracerebral hemorrhage features and SVD biomarkers.
146 0%) was the most common type of intracranial hemorrhage, followed by intracerebral hemorrhage (8%), a
147 thalmitis, retinal detachment, and choroidal hemorrhage following EK procedures is low.
148  postoperative endophthalmitis and choroidal hemorrhage following EK was 0.03% and 0.05%, respectivel
149 ent is the third documented case of vitreous hemorrhage following whole-body vibration training, he i
150 ascular dysregulation may contribute to disc hemorrhage formation in ocular hypertension.
151 ifferentiation of small foci of intracranial hemorrhage from calcium and improved diagnostic accuracy
152 ifferentiation of small foci of intracranial hemorrhage from calcium.
153                                     Vitreous hemorrhage from proliferative diabetic retinopathy can c
154 g 205 adults with vison loss due to vitreous hemorrhage from proliferative diabetic retinopathy who w
155   Among participants whose eyes had vitreous hemorrhage from proliferative diabetic retinopathy, ther
156                      Acer2 deficiency causes hemorrhages from the maternal vasculature in the junctio
157 al [CI], 1.25-5.53), and greater distance of hemorrhages from the ONH (OR, 1.24; 95% CI, 0.97-1.59).
158 face area of hemorrhages and the distance of hemorrhages from the ONH.
159 placenta previa/abuptio placenta/ante-partum hemorrhage, further significant factors, more importantl
160 ithout TS, those with TS had a higher Fisher Hemorrhage Grade and a lower mean (+/-standard deviation
161                   All individual DR lesions (hemorrhage [H], microaneurysm [ma], cotton wool spot [CW
162 ve pancreatic fistula and postpancreatectomy hemorrhage had the greatest independent impact on mortal
163                     Six weeks later, retinal hemorrhages had substantially resolved, and there was op
164  eosinophilic pneumonia and diffuse alveolar hemorrhage, have also been reported.
165  Compared with the reference group, vitreous hemorrhage (hazard ratio, 2.53 [P < 0.001] and 2.80 [P =
166 : 1.09 to 1.46; p = 0.0017) and intracranial hemorrhage (HR: 1.30; 95% CI: 1.07 to 1.59; p = 0.0094).
167  Participants at increased risk for variceal hemorrhage (HVPG >=12 mm Hg) had a higher mean SHAPE gra
168          Rates of secondary intraventricular hemorrhage, hydrocephalus, and thromboembolic events wer
169                                Intracerebral hemorrhage (ICH) accounts for a disproportionate amount
170 for supratentorial spontaneous intracerebral hemorrhage (ICH) and whether it is modified by key basel
171 MCE), ischemic stroke (IS) and intracerebral hemorrhage (ICH) in a cohort of Chinese adults.
172                                Intracerebral hemorrhage (ICH) is a devastating form of stroke affecti
173               Spontaneous deep intracerebral hemorrhage (ICH) is a devastating subtype of stroke with
174                                Intracerebral hemorrhage (ICH) is an especially feared complication in
175 BIs), multiple sclerosis (MS), intracerebral hemorrhage (ICH), and neuromyelitis optica (NMO).
176 cholesterol levels and risk of intracerebral hemorrhage (ICH), but it remains unclear whether this as
177 SCs) transplantation following intracerebral hemorrhage (ICH).
178 nt in patients presenting with intracerebral hemorrhage (ICH).
179 s emerged as a risk factor for intracerebral hemorrhage (ICH).
180 eir anticoagulant effects after intracranial hemorrhage (ICH).
181 el of hematoma clearance after intracerebral hemorrhage [ICH]), and (3) reduced proinflammatory respo
182 g Accelerated Resolution of Intraventricular Hemorrhage III trial and the Minimally Invasive Surgery
183 ion (aDelta: -1.00, P = 0.024), and vitreous hemorrhage in at least 1 eye (aDelta: -1.92, P = 0.021)
184  symptoms and prevention of life-threatening hemorrhage in immune thrombocytopenia (ITP) must be bala
185 ith higher rates of symptomatic intracranial hemorrhage in M2 occlusions only (OR = 4.40; 95% CI = 2.
186 gnesium levels are associated with extent of hemorrhage in patients with aneurysmal subarachnoid hemo
187  the treatment of gastro-esophageal variceal hemorrhage in patients with decompensated cirrhosis (fir
188 ive failure of clots decreases survival from hemorrhage in vivo.
189 s protective without increasing interstitial hemorrhages in the inflamed bowel or other organs.
190  to 30 [death]), progression of intracranial hemorrhage, incidence of seizures, and incidence of thro
191 primary and secondary prevention of cerebral hemorrhage include the treatment of hypertension, reduct
192 athology causing pulmonary consolidation and hemorrhage, increased mortality and specific modificatio
193 ear death and dependence after intracerebral hemorrhage, independent of known predictors of outcome.
194  microvascular obstruction (MVO), myocardial hemorrhage, infarct size, and clinical outcomes, after S
195 ot CFR, were associated with MVO, myocardial hemorrhage, infarct size, and clinical outcomes.
196 plications (i.e., endophthalmitis, choroidal hemorrhage, infectious keratitis, cystoid macular edema
197 e surface structure, presence of intraplaque hemorrhage (IPH), circle of Willis collaterals, and the
198           The efficient resolution of tissue hemorrhage is an important homeostatic function.
199 e findings suggest that intraretinal macular hemorrhage is an important indicator of disease severity
200                      Noncompressible truncal hemorrhage is the leading cause of potentially preventab
201 rtant neurologic complications: intracranial hemorrhage, ischemic stroke, and/or brain death, as a co
202 cardiopulmonary disease) and uDCD (including hemorrhage, major polytrauma, burns, and poisoning).
203 ve pancreatic fistula and postpancreatectomy hemorrhage may have the greatest impact on in-hospital m
204 r, hypoxia/reoxygenation (H/R), our in vitro hemorrhage model, increased miR-19b expression in human
205  bleeding is the main cause of postoperative hemorrhage, most often no actively bleeding vessel can b
206 tion, contusion, diarrhea, peripheral edema, hemorrhage, muscle spasms, and pneumonia, as well as adv
207 ere irritation (n = 312) and subconjunctival hemorrhage (n = 284).
208 ing conjunctival hemorrhage (n = 5), retinal hemorrhage (n = 4), and vitreous floaters (n = 4).
209 participants (16/21), including conjunctival hemorrhage (n = 5), retinal hemorrhage (n = 4), and vitr
210 ration (n = 17), death (n = 13), retrobulbar hemorrhage (n = 7), optic nerve damage (n = 4), vascular
211 to only 5% in isolated deep intraparenchymal hemorrhage not extending to cortex/insula, subarachnoid,
212                                   Submacular hemorrhage occurred in 15 patients (36%) who were treatm
213  the control group; symptomatic intracranial hemorrhage occurred in 4.5% of the patients in each grou
214                    Asymptomatic intracranial hemorrhage occurred in 51.4% of the patients in the thro
215 zures are frequent in lobar intraparenchymal hemorrhage, occurring in one in six monitored patients,
216 0.77; p = 0.011) and with thick subarachnoid hemorrhage (odds ratio 0.29 per 1 mg/dL increase; 95% CI
217 ter initial PPV were preoperative subretinal hemorrhage (odds ratio [OR], 5.73; P = 0.03), PVR found
218 r cohort presenting with delayed anastomotic hemorrhage of the donor duodenum (2.5%).
219 ed SPK transplant patients, with anastomotic hemorrhage of the donor duodenum as a very late complica
220 treat population of HARBOR were analyzed for hemorrhage on DFE or fundus photography and exudative ac
221 e evaluated for 82 patients with evidence of hemorrhage on DFE or fundus photography at 3 months and
222  with resolution of vitreous and pre-retinal hemorrhages on 4-month follow up.
223                    Small focal intracerebral hemorrhages only visible on exquisitely sensitive MRI se
224 ere normal, with no evidence of intracranial hemorrhage or edema.
225 ere normal, with no evidence of intracranial hemorrhage or edema.Her subsequent hospital course was c
226 fety outcome was a composite of intracranial hemorrhage or gastrointestinal bleeding.
227 outcomes included secondary intraventricular hemorrhage or hydrocephalus upon follow-up CT, thromboem
228  and lung disease that presents as pulmonary hemorrhage or interstitial lung disease (ILD).
229 was associated with symptomatic intracranial hemorrhage (OR = 3.01; 95% CI = 1.77-5.11; p < 0.0001).
230 d as seizures, ischemic stroke, intracranial hemorrhage, or brain death.Measurements and Main Results
231 as hepatic decompensation (ascites, variceal hemorrhage, or encephalopathy).
232 Subretinal hyperreflective material, macular hemorrhage, or RPE tear occurred in 14 of 47, 13 of 47,
233 hickness (P = 0.01) and presence of vitreous hemorrhage (P = 0.05).
234 17% of lobar and 5% of deep intraparenchymal hemorrhage (p = 0.09).
235 .57; 95% CI, 1.39-1.77) and in intracerebral hemorrhage patients compared with these groups (adjusted
236 ient among ischemic stroke and intracerebral hemorrhage patients stabilized.
237 ity in patients with aneurysmal subarachnoid hemorrhage, potentially through a hemostatic mechanism.
238 d gastric emptying (DGE), postpancreatectomy hemorrhage (PPH), bile leak, blood loss, reoperation, re
239 vement (p < 0.0001) had concomitant vitreous hemorrhage pre-op.
240 53 [95% CI, 0.05-1.02]; P=0.031), myocardial hemorrhage presence (odds ratio [OR], 3.20 [95% CI, 1.25
241 5% CI, -0.97 to -0.23]; P=0.002), myocardial hemorrhage presence (OR, 0.34 [95% CI, 0.15-0.75]; P=0.0
242  gains over 24 months, regardless of month 3 hemorrhage presence versus absence: 9.4 and 8.7 Early Tr
243 neumonia, serious infections, any infection, hemorrhage, renal failure, deep vein thrombosis, and unc
244  infection, liver diseases, gastrointestinal hemorrhage, renal failure, urinary tract calculus, chron
245 DR-related complications (including vitreous hemorrhage, retinal detachment, and neovascular glaucoma
246 d (kappa = 0.61, 0.48, and 0.52 for vitreous hemorrhage, retinal detachment, and neovascular glaucoma
247 rating room, endophthalmitis, suprachoroidal hemorrhage, retinal detachment, retinal tear, macular ed
248 e retina can explain the patterns of retinal hemorrhage (RH) seen in AHT.
249 patterns consistent with the diffuse retinal hemorrhages (RH) typically found in the posterior pole a
250 anial aneurysms (IA) and suffer subarachnoid hemorrhage (SAH) at younger ages than the general popula
251 ntribute to the pathogenesis of subarachnoid hemorrhage (SAH).
252 .0 [SD 18.4], 62% male, median intracerebral hemorrhage score 1.5 [interquartile range 1-2], delirium
253                          Background Subdural hemorrhage (SDH) is thought to have a benign course in a
254 ing deaths, 292 (44.4%) were P/PP; of these, hemorrhage, sepsis, and traumatic brain injury accounted
255  of retinopathy of prematurity, intracranial hemorrhage, sepsis, necrotizing enterocolitis, bronchopu
256 ort the hypothesis that magnesium influences hemorrhage severity in patients with aneurysmal subarach
257 erum magnesium and radiographic subarachnoid hemorrhage severity.
258 t shock pulmonary endothelial dysfunction in hemorrhage shock.
259 ssociated with high symptomatic intracranial hemorrhage (sICH) (24%) and mortality (53%) rates.
260 nical thrombectomy, symptomatic intracranial hemorrhage (sICH), and favorable outcome (modified Ranki
261 systemic embolism, symptomatic intracerebral hemorrhage (sICH), and major extracranial hemorrhage (EC
262 ects of the initial injury like swelling and hemorrhaging, strategies for the induction of neuronal r
263 of preclinical and clinical nonintracerebral hemorrhage studies, adjunct 1-deamino-8-D-arginine vasop
264 taset is composed of annotations of the five hemorrhage subtypes (subarachnoid, intraventricular, sub
265 outcomes in an animal model of intracerebral hemorrhage, suggesting that this process could have biol
266 yos had fewer visible blood vessels and more hemorrhages than their wild-type littermates, which was
267 lateral lung ischemia from t = 0-70 min plus hemorrhage to a mean arterial blood pressure (MAP) of 30
268 ar, subdural, epidural, and intraparenchymal hemorrhage) typically encountered at brain CT.
269            Adult patients with intracerebral hemorrhage under antiplatelet treatment and follow-up CT
270 ion (2 U) within 60 minutes of intracerebral hemorrhage under antiplatelet treatment diagnosis on bra
271  early platelet transfusion in intracerebral hemorrhage under antiplatelet treatment.
272 and dichotomized (thick vs thin subarachnoid hemorrhage) univariate and adjusted logistic regression
273 underwent splenectomy followed by controlled hemorrhage until lactate reached 7.5-8.5 mmol/L.
274 = 4-6) 1 year after first-ever intracerebral hemorrhage using logistic regression, adjusting for know
275 ersus early vitrectomy for diabetic vitreous hemorrhage (VH).
276  temporal lobe involvement, intraparenchymal hemorrhage volume, and electrographic seizures predicted
277     The 30-day cumulative incidence of major hemorrhage was 0.7% (95% CI, 0.1-5.1) and of clinically
278                                     Vitreous hemorrhage was a risk factor for earlier retinal breaks
279                            Extent of initial hemorrhage was graded semi-quantitatively on admission C
280                     Mild chronic parenchymal hemorrhage was noted in 3 left superior PV lobes after I
281 cted on SD-OCT in more than 89% of eyes when hemorrhage was present on DFE or fundus photography.
282 T detected nAMD activity in 89% of eyes when hemorrhage was present on fundus photography.
283  vision gains with or without injection when hemorrhage was present without OCT-detectable fluid.
284 e elevated risk for symptomatic intracranial hemorrhage was seen only within the first 14 days (16.3%
285      Bilateral disease, higher IOP, and disc hemorrhage were confirmed as risk factors for deteriorat
286 stenosis, plaque ulceration, and intraplaque hemorrhage were not associated with symptomatic status.(
287 oration of tympanic membranes and middle ear hemorrhage were observed at 1 and 7 days, and were resto
288 genation patients, the rates of intracranial hemorrhage were similar between venoarterial extracorpor
289                                      Retinal hemorrhages were categorized according to size-those sma
290 ural effusion, pneumothoraces or perihepatic hemorrhages were relatively easy to treat.
291 at lung syndecan-1 mRNA is reduced following hemorrhage, whereas the molecular mechanism underlying t
292  with later (2010-2013) measures of infarct, hemorrhage, white matter hyperintensity (WMH) grade, bra
293 ith intracerebral, subarachnoid, or subdural hemorrhages who had at least 1 follow-up image within 24
294 ion of clearance of VH and rate of recurrent hemorrhage with any additional treatment in both groups.
295 barachnoid hemorrhage; 4, thick subarachnoid hemorrhage with intraventricular hemorrhage).
296 ubarachnoid hemorrhage; 2, thin subarachnoid hemorrhage with intraventricular hemorrhage; 3, thick [>
297 e association of a retinal tear and vitreous hemorrhage with whole-body vibration training.
298 gest that the rapid accumulation of cerebral hemorrhages, with accompanying fluid egress, may cause f
299 rovement at 3 days; symptomatic intracranial hemorrhage within 36 hours; and all-cause death.
300                   This suggests that macular hemorrhages without OCT-detectable macular fluid may not

 
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