ライフサイエンスコーパス: intracranial hemorrhage

1 sed risks of hospitalization for bleeding or intracranial hemorrhage.

2 n oral anticoagulant treatment with incident intracranial hemorrhage.

3 presenting the risk of thrombolytic-related intracranial hemorrhage.

4 und to be relatively safe, with no excess in intracranial hemorrhage.

5 ticoagulation does not increase the risk for intracranial hemorrhage.

6 reatment, or antiplatelet therapy) after the intracranial hemorrhage.

7 did not show increased risk of developmental intracranial hemorrhage.

8 ent with occult brain metastasis had grade 4 intracranial hemorrhage.

9 All these agents reduced intracranial hemorrhage.

10 ted a significant predictive performance for intracranial hemorrhage.

11 sk of moderate or severe bleeding, including intracranial hemorrhage.

12 urrent stroke, including ischemic stroke and intracranial hemorrhage.

13 MAIN OUTCOME MEASURE: Symptomatic intracranial hemorrhage.

14 ith a history of stroke owing to the risk of intracranial hemorrhage.

15 reased the risk of major bleeding, including intracranial hemorrhage.

16 group (88% vs. 16%, p< 0.001) and 31% had an intracranial hemorrhage.

17 hemorrhage were compared with those without intracranial hemorrhage.

18 If severe, the thrombocytopenia can lead to intracranial hemorrhage.

19 improved with increasing risk for stroke and intracranial hemorrhage.

20 sequence for the detection of acute and old intracranial hemorrhage.

21 rnal platelet antigens and can lead to fetal intracranial hemorrhage.

22 ous abortion, and a high rate of spontaneous intracranial hemorrhage.

23 activity possibly contributory to brain AVM intracranial hemorrhage.

24 veness and safety in antiplatelet-associated intracranial hemorrhage.

25 but was modestly predictive in patients with intracranial hemorrhage.

26 ls to alert physicians to the possibility of intracranial hemorrhage.

27 gic outcomes; and 3) factors associated with intracranial hemorrhage.

28 48.0% specific (95% CI, 47.3-48.9) for acute intracranial hemorrhage.

29 hemoglobin, can identify infants with acute intracranial hemorrhage.

30 l support, are independently associated with intracranial hemorrhage.

31 lities, isolated skull fractures, or chronic intracranial hemorrhage.

32 %; P = .87), and total (44% vs 37%; P = .13) intracranial hemorrhages.

33 creased rate of recurrent cardiac events and intracranial hemorrhages.

34 ortality (9% vs. 12%, P=0.50) or symptomatic intracranial hemorrhage (0% vs. 3%, P=0.12).

35 .11; P=0.44), with significant reductions in intracranial hemorrhage (0.5% vs. 0.7%, P=0.02) and fata

36 ajor bleeding (2.2% vs. 0.6%, p < 0.001) and intracranial hemorrhage (0.6% vs. 0.1%, p = 0.015) witho

37 bypass grafting (2.1% vs. 0.6%, P<0.001) and intracranial hemorrhage (0.6% vs. 0.2%, P=0.009), withou

38 ajor bleeding event; 31 of these events were intracranial hemorrhages (0.8%/year).

39 follows: ischemic stroke, 0.80 (0.67-0.96); intracranial hemorrhage, 0.34 (0.26-0.46); major gastroi

40 Symptomatic intracranial hemorrhage (1% vs 4%) and parenchymal hemor

41 monary embolism (12.1% versus 7.8%; P=0.02), intracranial hemorrhage (1.6% versus 0.2%; P=0.03), and

42 t complications were infrequent: symptomatic intracranial hemorrhage, 1.8%; life-threatening or serio

43 to a congenital disorder developed an acute intracranial hemorrhage 10 days after surgery.

44 and brain trauma (29% [CI, 19% to 38%]), and intracranial hemorrhage (11% [CI, 7.7% to 14%]) were the

45 a lower rate of gastrointestinal bleeding or intracranial hemorrhage (12.9 per 1000 person-years) com

46 I, -2.5 to 0.7]; P = .29), or progression of intracranial hemorrhage (16% vs 20%; difference, -5.4% [

47 in-hospital deaths, 2873 (4.9%) patients had intracranial hemorrhage, 19,491 (33.4%) patients achieve

48 rain imaging, we sought 1) the prevalence of intracranial hemorrhage; 2) survival and neurologic outc

49 xic-ischemic brain injury (44%), followed by intracranial hemorrhage (24%), and ischemic infarct (16%

50 of seizures (1.1%), ischemic stroke (1.9%), intracranial hemorrhage (3.5%), and brain death (1.6%).

51 ted in 356 patients (7.1%), and included 181 intracranial hemorrhage (42.5%), 100 brain deaths (23.5%

52 codes for ischemic stroke (433-434, 436) and intracranial hemorrhage (430-432) identified 1812 stroke

53 h survival between patients with and without intracranial hemorrhage (68.3% vs 76.0%; p = 0.350).

54 injury; mortality was 79.6% in patients with intracranial hemorrhage, 68.2% in patients with stroke,

55 .7% [95% CI, -5.6% to 11.0%]) or symptomatic intracranial hemorrhage (7 [4.7%] vs 2 [1.3%]; unadjuste

56 ere still more likely to develop symptomatic intracranial hemorrhage (7.0% versus 5.7%; adjusted odds

57 had a higher unadjusted risk for symptomatic intracranial hemorrhage (7.7% versus 4.8%) and in-hospit

58 The main cause of brain injury was an intracranial hemorrhage (72%).

59 of death, nonfatal reinfarction, or nonfatal intracranial hemorrhage (a measure of net clinical benef

60 [95% CI: 1.31 to 1.97]) and greater risk of intracranial hemorrhage (adjusted HR: 2.04 [95% CI: 1.25

61 ot associated with risk-adjusted symptomatic intracranial hemorrhage (adjusted odds ratio, 1.0; 95% c

62 R = 1.24, 95% CI = 0.89-1.74) or symptomatic intracranial hemorrhage (adjusted OR = 0.87, 95% CI = 0.

63 There was 1 death from intracranial hemorrhage after coronary artery dissection

64 age, and nonwhite race, all risk factors for intracranial hemorrhage after fibrinolytic therapy, were

65 ociated with lower in-hospital mortality and intracranial hemorrhage, along with an increase in the p

66 ospital risk-adjusted mortality, symptomatic intracranial hemorrhage, ambulatory status at discharge,

67 time and in-hospital mortality, symptomatic intracranial hemorrhage, ambulatory status at discharge,

68 .1%, 29.6%, and 25.2%, respectively), severe intracranial hemorrhage among survivors (23.3%, 19.1%, a

69 tinal bleeding and 98 (32.6%) presented with intracranial hemorrhage; among the patients who could be

70 -year-old extended criteria donor died of an intracranial hemorrhage and had undergone cardiopulmonar

71 platelet antigen-1a (HPA-1a), can result in intracranial hemorrhage and intrauterine death.

72 The management of intracranial hemorrhage and intraventricular hemorrhage

73 Acute intracranial hemorrhage and intraventricular hemorrhage

74 Patients with intracranial hemorrhage and intraventricular hemorrhage

75 ansion and limit the medical consequences of intracranial hemorrhage and intraventricular hemorrhage.

76 information pertaining to the acute care of intracranial hemorrhage and intraventricular hemorrhage.

77 hibitors were associated with lower rates of intracranial hemorrhage and mortality compared with warf

78 rebral artery occlusion leading to increased intracranial hemorrhage and mortality.

79 e as monitored warfarin, with lower rates of intracranial hemorrhage and reduced mortality.

80 Primary outcomes evaluated were symptomatic intracranial hemorrhage and serious systemic hemorrhage;

81 common conditions associated with LRDA were intracranial hemorrhage and subarachnoid hemorrhage.

82 ies; 28% to 43% and 1% to 30%, respectively) intracranial hemorrhage and vessel perforation or dissec

83 iated through a reduction in rates of severe intracranial hemorrhage and/or cystic periventricular le

84 ANS-associated reductions in rates of severe intracranial hemorrhage and/or cystic periventricular le

85 ockdown of a zebrafish ADA2 homologue caused intracranial hemorrhages and neutropenia - phenotypes th

86 leeding (blood loss requiring transfusion or intracranial hemorrhage) and thrombosis during ECMO supp

87 , 2.20 (95% CI: 1.26, 3.84) for nontraumatic intracranial hemorrhage, and 2.17 (95% CI: 1.60, 2.96) f

88 s during acute traumatic brain injury, acute intracranial hemorrhage, and acutely growing brain tumor

89 sk for ischemic stroke or systemic embolism, intracranial hemorrhage, and all-cause mortality without

90 ification of examinations positive for acute intracranial hemorrhage, and also exceeded the performan

91 subluxations and/or dislocations, fractures, intracranial hemorrhage, and arterial injury.

92 ity fracture, pelvic fracture, central line, intracranial hemorrhage, and blood transfusion).

93 ciated with reduced risk of ischemic stroke, intracranial hemorrhage, and death and increased risk of

94 Ischemic stroke, intracranial hemorrhage, and death.

95 iated with reduced mortality and symptomatic intracranial hemorrhage, and higher rates of independent

96 unctional outcome, lower odds of symptomatic intracranial hemorrhage, and lower odds of requirement f

97 a group, NOACs significantly reduce stroke, intracranial hemorrhage, and mortality, with lower to si

98 Risks of all-cause mortality, intracranial hemorrhage, and parenchymal hematoma at 90

99 There were no reports of intracranial hemorrhage, and the most common site of ble

100 eviewed for the presence of skull fractures, intracranial hemorrhage, and traumatic DVST.

101 h, myocardial infarction, major bleeding, or intracranial hemorrhage as an outcome.

102 anticoagulant treatment reintroduction after intracranial hemorrhage as feasible.

103 To assess the risk for intracranial hemorrhage associated with the administrati

104 nces observed in the cumulative incidence of intracranial hemorrhage at 1 year in the enoxaparin and

105 Intracranial hemorrhage at diagnosis was rare (0.6%).

106 Sixteen patients (12.2%) had evidence of intracranial hemorrhage at or near the time of diagnosis

107 Intracranial hemorrhage at presentation was defined as t

108 systemic emboli prevented by warfarin minus intracranial hemorrhages attributable to warfarin, multi

109 opressin (DDAVP) for antiplatelet-associated intracranial hemorrhage based on low-quality evidence.

110 ban increased the risk of major bleeding and intracranial hemorrhage but not the risk of fatal bleedi

111 tely increase or decrease the probability of intracranial hemorrhage, but no finding or combination o

112 ted a significant predictive performance for intracranial hemorrhage (c-index: 0.75; p = 0.03).

113 gastrointestinal, or genitourinary bleeding; intracranial hemorrhage; cardiac tamponade; nonbypass su

114 high risk for hypoxic-ischemic brain injury, intracranial hemorrhage, cerebral edema, and brain death

115 nfection, bronchopulmonary dysplasia, severe intracranial hemorrhage, cystic periventricular leukomal

116 The rates of intracerebral and intracranial hemorrhage did not differ significantly bet

117 The rate of symptomatic intracranial hemorrhage did not differ significantly bet

118 However, massive intracranial hemorrhage distinguishes these patients fro

119 When intracranial hemorrhage does occur, it is often due to o

120 f 0-2) and mortality at 90 days, symptomatic intracranial hemorrhage, emboli to new territory, and va

121 Intracranial hemorrhage events associated with NOACs in

122 anagement of minimally injured patients with intracranial hemorrhage exclusively by trauma surgeons.

123 study identified two quantitative markers of intracranial hemorrhage expansion at dual-energy CT of t

124 as associated with a decreased likelihood of intracranial hemorrhage expansion during the first 24 ho

125 associated with 88% decreased likelihood of intracranial hemorrhage expansion during the first 24 ho

126 Primary effectiveness outcome was intracranial hemorrhage expansion greater than or equal

127 Ischemic stroke, intracranial hemorrhage, extracranial bleeding, and myoc

128 hemorrhage (20%) was the most common type of intracranial hemorrhage, followed by intracerebral hemor

129 ensitive to the rates of ischemic stroke and intracranial hemorrhage for LAA closure and medical anti

130 ion, the adjusted odds ratio for symptomatic intracranial hemorrhage for those on NOACs was 0.92 (95%

131 In patients with VKA-related intracranial hemorrhage, four-factor PCC might be superi

132 ance in the differentiation of small foci of intracranial hemorrhage from calcium and improved diagno

133 y CT in the differentiation of small foci of intracranial hemorrhage from calcium.

134 re referred for dual-energy CT assessment of intracranial hemorrhage from October 2014 to January 201

135 e of major bleeding is gastrointestinal, but intracranial hemorrhage has the worst prognosis.

136 c brain injury, subarachnoid hemorrhage, and intracranial hemorrhage have demonstrated that prolonged

137 atio, 1.15; 95% CI, 1.00 to 1.32), including intracranial hemorrhage (hazard ratio, 1.42; 95% CI, 1.1

138 These findings included intracranial hemorrhages, hemorrhages involving the opti

139 were safer with respect to the reduction of intracranial hemorrhage (HR, 0.38; 95% CI, 0.26-0.56).

140 1.26; 95% CI: 1.09 to 1.46; p = 0.0017) and intracranial hemorrhage (HR: 1.30; 95% CI: 1.07 to 1.59;

141 onade (HR: 2.38 [95% CI: 0.56 to 10.1]), and intracranial hemorrhage (HRs for 1-year mortality were n

142 The risk of further intracranial hemorrhage (ICH) and the benefit of stroke

143 dy racial/ethnic differences in the risk for intracranial hemorrhage (ICH) and the effect of warfarin

144 The risks of major bleeding and intracranial hemorrhage (ICH) are higher in Asian patien

145 agnostic performance of APT MRI in detecting intracranial hemorrhage (ICH) at hyperacute, acute and s

146 ine learning: body region identification and intracranial hemorrhage (ICH) detection.

147 Estimating risk of intracranial hemorrhage (ICH) for patients with unruptur

148 eports of statin usage and increased risk of intracranial hemorrhage (ICH) have been inconsistent.

149 nticoagulation does not increase the risk of intracranial hemorrhage (ICH) in patients with solid tum

150 Intracranial hemorrhage (ICH) is a rare but devastating

151 Spontaneous intracranial hemorrhage (ICH) is also a frequent occurre

152 NAIT) is a life-threatening disease in which intracranial hemorrhage (ICH) is the major risk.

153 uloprotection was assessed as microbleed and intracranial hemorrhage (ICH) rates.

154 Intracranial hemorrhage (ICH) was the most common site o

155 mized studies have shown a decreased risk of intracranial hemorrhage (ICH) with use of novel oral ant

156 SSRIs) may increase the risk for spontaneous intracranial hemorrhage (ICH), an effect that is in theo

157 temic embolic events (SSEE), major bleeding, intracranial hemorrhage (ICH), and all-cause death.

158 16, we compared the risk of ischemic stroke, intracranial hemorrhage (ICH), hospitalization for gastr

159 We assessed ACT-associated intracranial hemorrhage (ICH), including frequency, clin

160 tigated the frequency and characteristics of intracranial hemorrhage (ICH), the factors associated wi

161 results in a sequence of events that lead to intracranial hemorrhage (ICH).

162 outcomes were risk of recurrent embolism and intracranial hemorrhage (ICH).

163 neutralize their anticoagulant effects after intracranial hemorrhage (ICH).

164 Epidemiological data on the risk of intracranial hemorrhage (ICrH) after ischemic stroke are

165 eritis nodosa, lacunar ischemic strokes, and intracranial hemorrhages), immunodeficiency and bone mar

166 Bleeding occurred in 70.2%, including intracranial hemorrhage in 16%, and was independently as

167 was cerebral ischemia in 73.3% of patients, intracranial hemorrhage in 22.8%, and a stroke-mimicking

168 of Hedgehog signaling increased the risk of intracranial hemorrhage in ciliary mutants, activation o

169 As a potential treatment to prevent fetal intracranial hemorrhage in HPA-1a alloimmunized pregnanc

170 brain pericytes are associated with neonatal intracranial hemorrhage in human fetuses, as well as str

171 A mathematical model that can predict acute intracranial hemorrhage in infants at increased risk of

172 Accurate and timely identification of intracranial hemorrhage in infants without a history of

173 associated with higher rates of symptomatic intracranial hemorrhage in M2 occlusions only (OR = 4.40

174 ilar or reduced rates of ischemic stroke and intracranial hemorrhage in patients with AF compared wit

175 Early reperfusion was associated with fatal intracranial hemorrhage in patients with the Malignant p

176 Hypernatremia is associated with intracranial hemorrhage in term infants.

177 Four were symptomatic, including fatal intracranial hemorrhage in the index case.

178 Unadjusted rates of symptomatic intracranial hemorrhage in the NOAC, warfarin, and none

179 There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs

180 e basis of a multivariable model to identify intracranial hemorrhage in well-appearing infants using

181 There were more intracranial hemorrhages in the tenecteplase group.

182 ompared with warfarin for any outcome except intracranial hemorrhage, in which case dabigatran risk w

183 o disability] to 30 [death]), progression of intracranial hemorrhage, incidence of seizures, and inci

184 factors were identified in association with intracranial hemorrhage, including age at initial diagno

185 emorrhagic effect of NAC in a mouse model of intracranial hemorrhage induced by in situ collagenase t

186 It is unclear whether intracranial hemorrhage is a consequence of the extracor

187 real membrane oxygenation, the occurrence of intracranial hemorrhage is associated with a high mortal

188 torative therapy, as the risk for triggering intracranial hemorrhage is eliminated and tPA-S478A can

189 We conclude that intracranial hemorrhage is frequently observed in patien

190 Symptomatic intracranial hemorrhage is infrequent, but approximately

191 Intracranial hemorrhage is the most feared complication

192 ted with important neurologic complications: intracranial hemorrhage, ischemic stroke, and/or brain d

193 were included when subarachnoid hemorrhage, intracranial hemorrhage, ischemic stroke, sub/epidural h

194 Patients with trauma, intracranial hemorrhage known prior to arrival, or witho

195 red with warfarin, was associated with fewer intracranial hemorrhages, less adverse consequences foll

196 Treatment complications included symptomatic intracranial hemorrhage, life-threatening or serious sys

197 Our findings suggest that intracranial hemorrhage may not be an infrequent occurre

198 ggest that the IL-6 genotype associated with intracranial hemorrhage modulates IL-6 expression in bra

199 For intracranial hemorrhage, mortality was not improved with

200 sk for ischemic stroke or systemic embolism, intracranial hemorrhage, myocardial infarction, or morta

201 versible encephalopathy syndrome, n = 1; and intracranial hemorrhage, n = 1).

202 Symptomatic intracranial hemorrhage occurred in 2 patients (5%).

203 % of those in the control group; symptomatic intracranial hemorrhage occurred in 4.5% of the patients

204 Asymptomatic intracranial hemorrhage occurred in 51.4% of the patient

205 More intracranial hemorrhages occurred in the fibrinolysis gr

206 efined as brain death, seizures, stroke, and intracranial hemorrhage occurring during extracorporeal

207 Intracranial hemorrhage occurs in 0.5-1.0% of affected c

208 ts were preserved when weighting factors for intracranial hemorrhage of 1.0 and 2.0 were used.

209 th and low birth weight, birth asphyxia, and intracranial hemorrhage of the newborn significantly dec

210 ly confirmed single spontaneous or traumatic intracranial hemorrhage, of whom 39 (83%) had hearing lo

211 logically confirmed spontaneous or traumatic intracranial hemorrhage, of whom none had hearing loss,

212 with TBI (findings of skull fracture and/or intracranial hemorrhage on an initial computed tomograph

213 resenting history and documented evidence of intracranial hemorrhage on cerebral CT scan were include

214 ase on all patients with TBI (skull fracture/intracranial hemorrhage on head computed tomography) pre

215 ome measures were findings of progression of intracranial hemorrhage on repeated computed tomographic

216 9 patients [16.6%]; P = .89), progression of intracranial hemorrhage on repeated scans (post-BIG grou

217 but no significant difference in symptomatic intracranial hemorrhage or all-cause mortality at 90 day

218 (not shown) were normal, with no evidence of intracranial hemorrhage or edema.

219 (not shown) were normal, with no evidence of intracranial hemorrhage or edema.Her subsequent hospital

220 he primary safety outcome was a composite of intracranial hemorrhage or gastrointestinal bleeding.

221 department visit with a primary diagnosis of intracranial hemorrhage or gastrointestinal, urogenital,

222 d with higher unadjusted odds of symptomatic intracranial hemorrhage or serious systemic hemorrhage,

223 = 0.76), but was associated with symptomatic intracranial hemorrhage (OR = 3.01; 95% CI = 1.77-5.11;

224 ity (OR, 1.40; 95% CI: 0.37, 5.25; P = .62), intracranial hemorrhage (OR, 0.55; 95% CI: 0.03, 8.91; P

225 I, 0.95-0.98; P < .001), reduced symptomatic intracranial hemorrhage (OR, 0.96; 95% CI, 0.95-0.98; P

226 tions, defined as seizures, ischemic stroke, intracranial hemorrhage, or brain death.Measurements and

227 pendently associated with older patient age, intracranial hemorrhage (other than epidural), skull fra

228 m (p = 0.0004 and p = 0.0006, respectively), intracranial hemorrhage (p = 0.0007 and p = 0.0005, resp

229 imilar association was noted for the risk of intracranial hemorrhage (P=0.015) and progressive aortic

230 gic transformation (P=0.001) and symptomatic intracranial hemorrhage (P=0.036).

231 Subdural hematoma is a common type of intracranial hemorrhage, particularly among the elderly,

232 Secondary safety outcomes included severe intracranial hemorrhage, periventricular leukomalacia, a

233 nction, bacterial infection, length of stay, intracranial hemorrhage, periventricular leukomalacia, c

234 treatment reduced the combined end point of intracranial hemorrhage, periventricular leukomalacia, o

235 port genes in respective mutants rescued the intracranial hemorrhage phenotype.

236 crease the risk of aneurysm formation, acute intracranial hemorrhage, play a vital role in neurosurgi

237 s both risk for thromboembolism and risk for intracranial hemorrhage provides a more quantitatively i

238 rsus 1.5%; P=0.04) with a trend toward lower intracranial hemorrhage rates compared with low-volume c

239 Intracranial hemorrhage rates were 1.1% and 0.2%, respec

240 Stroke unit admission, symptomatic intracranial hemorrhage rates, and in-hospital mortality

241 d with lower in-hospital mortality and lower intracranial hemorrhage rates.

242 parable outcomes regarding the occurrence of intracranial hemorrhage, regardless of the antenatal man

243 Three patients had intracranial hemorrhages related to the intracranial pre

244 ents with atrial fibrillation who survive an intracranial hemorrhage remains unknown.

245 f life-saving treatments among patients with intracranial hemorrhage, representing a self-fulfilling

246 und Diagnostic uncertainty in CT of possible intracranial hemorrhage requires short-interval follow-u

247 neonatal complications, such as nontraumatic intracranial hemorrhage, respiratory distress syndrome,

248 ents (an absolute hemoglobin drop >/=4 g/dL, intracranial hemorrhage, retroperitoneal bleed, or trans

249 a consideration, but its risks of major and intracranial hemorrhages rival overall harms from interm

250 , 0.72-1.02) with a significant reduction of intracranial hemorrhage (RR, 0.46; 95% CI, 0.39-0.56).

251 ly no detectable differences in the risks of intracranial hemorrhage (RR, 1.15; 95% CI, 0.67-1.97; RD

252 in the rates of retinopathy of prematurity, intracranial hemorrhage, sepsis, necrotizing enterocolit

253 es, EVT was associated with high symptomatic intracranial hemorrhage (sICH) (24%) and mortality (53%)

254 p a score for assessing risk for symptomatic intracranial hemorrhage (sICH) in ischemic stroke patien

255 Symptomatic intracranial hemorrhage (sICH) was evaluated with Nation

256 of IVT/mechanical thrombectomy, symptomatic intracranial hemorrhage (sICH), and favorable outcome (m

257 ]) and destination at discharge, symptomatic intracranial hemorrhage (sICH), and in-hospital mortalit

258 Symptomatic intracranial hemorrhage (sICH), in-hospital mortality, d

259 The primary safety outcome was symptomatic intracranial hemorrhage (SICH); 3-month functional indep

260 the association between SaO and symptomatic intracranial hemorrhage (sICH, European Cooperative Acut

261 lin were favored in subarachnoid hemorrhage, intracranial hemorrhage, spine, demyelinating disease, a

262 We report a higher prevalence of intracranial hemorrhage than has previously been describ

263 significantly more likely to have died from intracranial hemorrhage than were all other deceased org

264 Compared with the 115 patients without intracranial hemorrhage, the 16 patients presenting with

265 rtality (per 100 person-years) for recurrent intracranial hemorrhage, the rate of ischemic stroke/sys

266 Adverse events (AEs), such as intracranial hemorrhage, thromboembolic event, and progr

267 ) recordings were averaged up to the time of intracranial hemorrhage, thromboembolic event, or progre

268 vealed factors independently associated with intracranial hemorrhage to be duration of ventilation (d

269 ents receiving antiplatelet therapy who have intracranial hemorrhage (traumatic or spontaneous).

270 nt at recognition of antiplatelet-associated intracranial hemorrhage versus nontreatment.

271 5, reflecting the greater clinical impact of intracranial hemorrhage versus thromboembolism.

272 Fatal bleeding or intracranial hemorrhage was 0.9% with both treatments in

273 The prevalence of intracranial hemorrhage was 16.4% in extracorporeal memb

274 rtality was 21%, and the rate of symptomatic intracranial hemorrhage was 4%; neither rate differed ac

275 The risk for intracranial hemorrhage was fourfold higher (adjusted ha

276 val, 0.69 to 0.90; P<0.0003) and symptomatic intracranial hemorrhage was less frequent (4.7% versus 5

277 The rate of symptomatic intracranial hemorrhage was lower in stroke mimics (0.4%

278 Intracranial hemorrhage was lower with higher-dose NOACs

279 Intracranial hemorrhage was noted in 2 neonates (nadir p

280 Intracranial hemorrhage was noted in two patients (2.4%)

281 me epochs, the elevated risk for symptomatic intracranial hemorrhage was seen only within the first 1

282 The risk of symptomatic intracranial hemorrhage was similar with either treatmen

283 Intracranial hemorrhage was the most frequent type, and

284 At 90 days, the rates of symptomatic intracranial hemorrhage were 1.9% in both the thrombecto

285 py, and outcomes in patients presenting with intracranial hemorrhage were compared with those without

286 hemorrhage, the 16 patients presenting with intracranial hemorrhage were more frequently women, less

287 Major bleeding and intracranial hemorrhage were similar between a pharmacoi

288 membrane oxygenation patients, the rates of intracranial hemorrhage were similar between venoarteria

289 w of radiographic imaging was performed, and intracranial hemorrhages were categorized as trace, meas

290 ial fractures, more severe injuries, such as intracranial hemorrhages, were associated with a higher

291 farin therapy may face an increased risk for intracranial hemorrhage when treated with tPA.

292 s, displayed increased risk of developmental intracranial hemorrhage, whereas the morphology of the v

293 tients at greatest risk of suffering a major intracranial hemorrhage with anticoagulation.

294 ble from warfarin except for a lower risk of intracranial hemorrhage with dabigatran.

295 [95% CI, 0.83-0.94], P < .001), symptomatic intracranial hemorrhage within 36 hours was less likely

296 rological improvement at 3 days; symptomatic intracranial hemorrhage within 36 hours; and all-cause d

297 Fatal or nonfatal symptomatic intracranial hemorrhage within 7 days occurred in 6% of

298 gnificant difference in rates of symptomatic intracranial hemorrhage within 90 days (70 events [5.7%]

299 c revascularization at 24 hours, symptomatic intracranial hemorrhage within 90 days, and all-cause mo

300 as obtained and demonstrated a left parietal intracranial hemorrhage without midline shift or hydroce