ライフサイエンスコーパス: haemorrhage

1 ry artery, myocardial infraction, and muscle haemorrhage).

2 e severe bleeding (traumatic and post-partum haemorrhage).

3 ncreasing the absolute risk of intracerebral haemorrhage).

4 er and/or neuroretinal rim defects, and disc haemorrhages).

5 or dependence by reducing the extent of the haemorrhage.

6 ntia and risk factors after an intracerebral haemorrhage.

7 aesarean births, infections, and post-partum haemorrhage.

8 m functional performance after intracerebral haemorrhage.

9 elivery, and are more at risk of post-partum haemorrhage.

10 surgery (MIS) in patients with intracerebral haemorrhage.

11 as a therapeutic strategy for intracerebral haemorrhage.

12 or community-level prophylaxis of postpartum haemorrhage.

13 ng antiplatelet therapy before intracerebral haemorrhage.

14 prove functional outcome after intracerebral haemorrhage.

15 grade patients after aneurysmal subarachnoid haemorrhage.

16 ts relevance in time-to-death in post-partum haemorrhage.

17 eath from bleeding in trauma and post-partum haemorrhage.

18 ominent feature of experimental subarachnoid haemorrhage.

19 cerebrovasculature, i.e. ischaemic stroke or haemorrhage.

20 ve of comorbidity, except for exsanguinating haemorrhage.

21 and no increase in symptomatic intracerebral haemorrhage.

22 placebo group withdrew because of abdominal haemorrhage.

23 in, other angina, and subdural or extradural haemorrhage.

24 ibrillation and one case of grade 3 or worse haemorrhage.

25 outcome in patients with acute intracerebral haemorrhage.

26 therapy or in the setting of a subarachnoid haemorrhage.

27 ome in patients with aneurysmal subarachnoid haemorrhage.

28 le >3) versus those with acute intracerebral haemorrhage.

29 ith probable CAA without lobar intracerebral haemorrhage.

30 ) in cesarean section among women at risk of haemorrhage.

31 ity related to uterine rupture and extensive haemorrhage.

32 st corrected visual acuity owing to vitreous haemorrhage.

33 haemorrhage size and thalamic intracerebral haemorrhage.

34 functional independence) after intracerebral haemorrhage.

35 e posterior pole, vascular abnormalities and haemorrhages.

36 al schisis with pre-retinal and intraretinal haemorrhages.

37 ection of gastrointestinal and head-and-neck haemorrhages.

38 a clinical consequence of perinatal cerebral haemorrhaging.

39 aneurysm (0.46 [0.35-0.59]) and subarachnoid haemorrhage (0.48 [0.26-0.89]), and not associated with

40 aneurysm (0.46, 0.35-0.59) and subarachnoid haemorrhage (0.48, 0.26-0.89).

41 (0.90, 0.85-0.95; p=0.0003) and intracranial haemorrhage (0.48, 0.39-0.59; p<0.0001), but increased g

42 in the intervention group), major obstetric haemorrhage (1% vs 3%), and small-for-gestational-age in

43 (1.68, 95% CI 1.60-1.77), and intracerebral haemorrhage (1.24, 95% CI 1.07-1.44).

44 age (1.49, 1.01-2.20; I(2)=37%), post-partum haemorrhage (1.29, 1.13-1.49; I(2)=41%), hypertensive di

45 ratio 1.44 [95% CI 1.32-1.58]), subarachnoid haemorrhage (1.43 [1.25-1.63]), and stable angina (1.41

46 .54, 95% CI 1.02-2.32; I(2)=67%), antepartum haemorrhage (1.49, 1.01-2.20; I(2)=37%), post-partum hae

47 bsolute excess 5.5% [4.6-6.4]); of SITS-MOST haemorrhage (124 [3.7%] of 3391 vs 19 [0.6%] of 3365; OR

48 sure was much lower than after intracerebral haemorrhage (158.5 mm Hg [SD 30.1] vs 189.8 mm Hg [38.5]

49 orrhage more than 1 year after their initial haemorrhage (17 from the target aneurysm).

50 lute increase in risk of fatal intracerebral haemorrhage (2.2% [1.5% to 3.0%]) and the increased risk

51 p<0.001), and more often with intracerebral haemorrhage (20% vs 13%, p=0.002).

52 /day], haemoptysis [80 mg/day], intracranial haemorrhage [20 mg/day], ventricular fibrillation [120 m

53 2 [19%] of 227 patients; p=0.0468) and major haemorrhage (29 [13%]of 224 patients vs 10 [4%] of 227 p

54 asm in patients with aneurysmal subarachnoid haemorrhage; (4) the use in the biomechanical assessment

55 3.1% [2.4-3.8]); and of fatal intracerebral haemorrhage (91 [2.7%] of 3391 vs 13 [0.4%] of 3365; OR

56 Subarachnoid haemorrhage, a particularly deadly form of intracranial

57 Haemorrhage accounted for 27.1% (661 000, 19.9-36.2), hy

58 Improvements in the control of haemorrhage after trauma have resulted in the survival o

59 , three in NightLyte (upper gastrointestinal haemorrhage, alcohol poisoning and related head injury,

60 PRETATION: In patients with intraventricular haemorrhage and a routine extraventricular drain, irriga

61 a largely untreatable cause of intracerebral haemorrhage and contributor to age-related cognitive dec

62 ents undergoing TIPSS insertion for variceal haemorrhage and correlate this with outcome.

63 orted on the risks of recurrent subarachnoid haemorrhage and death or dependency for a minimum of 5 y

64 all vessel disorder leading to intracerebral haemorrhage and dementia.

65 yses to assess mortality after intracerebral haemorrhage and examine the absolute risks of intracereb

66 -Cre transgenic mouse line, leads to oedema, haemorrhage and increased levels of embryonic lethality.

67 T cells in the context of tPA-induced brain haemorrhage and investigated the underlying mechanisms o

68 s for association with primary intracerebral haemorrhage and ischaemic stroke subtypes.

69 Primary intracerebral haemorrhage and lacunar ischaemic stroke are acute manif

70 , leading to increased primary intracerebral haemorrhage and lacunar stroke risk.

71 evels increase risk of primary intracerebral haemorrhage and lacunar stroke, directly implicate the m

72 ips was analysed over Days 0-3 after initial haemorrhage and magnetic resonance imaging studies were

73 dverse events (subconjunctival or subretinal haemorrhage and mild cell debris in the anterior vitreou

74 and lower rates of symptomatic intracranial haemorrhage and mortality, in patients with acute ischae

75 r permeability, development of intracerebral haemorrhage and neurovascular injury in experimental str

76 oss, decreased pulmonary function, pulmonary haemorrhage and pathological signs indicative of end-sta

77 atory evidence of an aneurysmal subarachnoid haemorrhage and presenting less than 96 h from ictus fro

78 evaluation of acute, active gastrointestinal haemorrhage and show its usefulness prior to embolizatio

79 ausing serious bleeding such as intracranial haemorrhage and the need for anticoagulation monitoring.

80 opposed to focal deficits after subarachnoid haemorrhage and traumatic brain injury in humans, axonal

81 mice is lethal due to multiple intracranial haemorrhages and brain blood vessels leakage.

82 indicated by elevated liver enzymes, mucosal haemorrhages and generalized petechia could be reversed,

83 ved adult heterozygous mice exhibit frequent haemorrhages and increased vascular permeability due to

84 DBS complications, with fewer intracerebral haemorrhages and infections with general anaesthesia (p<

85 or patients with non-CAA deep intracerebral haemorrhage) and patients with Alzheimer's disease.

86 or ischaemic stroke, 87.1% for intracerebral haemorrhage), and were consistent across regions (rangin

87 nine [<1%] vs seven [<1%]) had grade 3-5 CNS haemorrhage, and 40 (19 [1%] vs 21 [1%]) had grade 3-5 c

88 major bleeding, fatal bleeding, intracranial haemorrhage, and gastrointestinal bleeding.

89 ial infarction, major bleeding, intracranial haemorrhage, and gastrointestinal bleeding.

90 CI 10.0-19.3) at 1 year after intracerebral haemorrhage, and incidence reached 28.3% (22.4-34.5) at

91 gnificant reductions in stroke, intracranial haemorrhage, and mortality, and with similar major bleed

92 ) which occurs after aneurysmal subarachnoid haemorrhage, and often leads to cerebral infarction and

93 ey, airway management, chest injuries, major haemorrhage, and paediatric trauma.

94 ) had grade 3 pain, three (4%) had grade 3-4 haemorrhage, and three (4%) had gastrointestinal adverse

95 with ischaemic stroke and 3059 intracerebral haemorrhage] and 13 472 controls).

96 Delayed seizures after intracerebral haemorrhage are associated with different risk factors,

97 Paramount in the clot's capability to stem haemorrhage are its changing mechanical properties, the

98 in synergy with direct ischaemic effects of haemorrhage as mechanisms of infarct development.

99 prospective cohort studies with subarachnoid haemorrhage as outcome.

100 n in the context of ageing and intracerebral haemorrhage, as well as in Alzheimer's and other dementi

101 pasm (cVSP) in human aneurysmal subarachnoid haemorrhage (aSAH).

102 uced death or dependence after intracerebral haemorrhage associated with antiplatelet therapy use.

103 or endovascular coiling after a subarachnoid haemorrhage, assuming treatment equipoise, between Sept

104 Excessive haemorrhage at cesarean section requires donor (allogene

105 erebrospinal fluid leakage and intracerebral haemorrhage) at days 3-7 after AAV2 gene therapy, and we

106 riovenous malformation-related intracerebral haemorrhage (AVICH) score showed better outcome predicti

107 h at 712 deaths per 100 000 livebirths, with haemorrhage being the leading cause of death.

108 ms to be safe in patients with intracerebral haemorrhage, but increased asymptomatic bleeding is a ma

109 s outnumbered warfarin-related intracerebral haemorrhages by about 15-fold (280 vs 19), rising to 50-

110 ither incidence of symptomatic intracerebral haemorrhage (by SITS-MOST definition, 1/52 [2%] tenectep

111 .2-2.5 cm(3), p<0.0001) and irregular-shaped haemorrhages (by 4.8-4.9 cm(3), p<0.0001).

112 scovery cohort of 1409 primary intracerebral haemorrhage cases and 1624 controls from three studies,

113 Formal measurement of haemorrhage characteristics and visual estimates are rep

114 ntracerebral haemorrhage (ICH) is related to haemorrhage characteristics.

115 e each of renal failure, oesophageal varices haemorrhage, circulatory collapse, wound infection, ileu

116 Among many factors, delayed haemorrhage control and preload driven excessive use of

117 s (96 healthy elderly, 42 deep intracerebral haemorrhage controls) and 72 patients with Alzheimer's d

118 nfection, globe penetration, and peri-ocular haemorrhage could occur.

119 : Acute non-traumatic convexity subarachnoid haemorrhage (cSAH) is increasingly recognised in cerebra

120 l outcomes included symptomatic intracranial haemorrhage (defined by type 2 parenchymal haemorrhage w

121 intracranial haemorrhage (type 2 parenchymal haemorrhage definition 231 [6.8%] of 3391 vs 44 [1.3%] o

122 morrhage (hazard ratio 1.63, P = 0.036), pre-haemorrhage dementia (hazard ratio 1.36, P = 0.044), his

123 , we sought to understand the performance of haemorrhage descriptors in large clinical trials.

124 hymal haematoma and symptomatic intracranial haemorrhage did not differ between populations.

125 the significance of delayed intraventricular haemorrhage (dIVH) is less well defined.

126 the significance of delayed intraventricular haemorrhage (dIVH) is less well defined.

127 ema or with mild intraoperative pupil margin haemorrhage during anterior segment surgery.

128 nfarct sizes, cardiac fibrosis and necrosis, haemorrhages, edema, and macrophage density associated w

129 ] vs 35 [6%]) and grade 3 or worse pulmonary haemorrhage (eight [1%] vs eight [1%]) did not differ be

130 anaemia (eight [4%]), upper gastrointestinal haemorrhage (eight [4%]), pneumonia (seven [3%]), gastri

131 560 patients with spontaneous intracerebral haemorrhage enrolled in the PITCH cohort between Nov 3,

132 s 4/51 [8%], p=0.59) nor total intracerebral haemorrhage events (8/52 [15%] vs 14/51 [29%], p=0.091)

133 thin 7 days before randomisation, fever, and haemorrhage expected to require transfusion with up to t

134 , lacunar infarcts, microhaemorrhage, larger haemorrhage, fibrinoid necrosis, microaneurysms, perivas

135 haemorrhage (six [3%]), and gastrointestinal haemorrhage (five [2%]) in the trastuzumab emtansine 2.4

136 The relative increase in fatal intracranial haemorrhage from alteplase was similar irrespective of t

137 s with severe - sometimes life-threatening - haemorrhage from biliary ducts.

138 mpare favourably with the risks of recurrent haemorrhage from CCM.

139 y in patients with spontaneous intracerebral haemorrhage from the Prognosis of Intracerebral Haemorrh

140 ansfusion (primary outcome) and fetomaternal haemorrhage >/=2 ml in RhD-negative women with RhD-posit

141 od pressure were strongest for intracerebral haemorrhage (hazard ratio 1.44 [95% CI 1.32-1.58]), suba

142 zures included cortical involvement on index haemorrhage (hazard ratio 1.63, P = 0.036), pre-haemorrh

143 P = 0.044), history of multiple prior lobar haemorrhages (hazard ratio 2.50, P = 0.038), exclusively

144 Between 2003 and 2009, haemorrhage, hypertensive disorders, and sepsis were res

145 botic agents increase risks of intracerebral haemorrhage (ICH) and associated adverse outcomes.

146 d 2839 adults with spontaneous intracerebral haemorrhage (ICH) and high systolic blood pressure (150-

147 ip between laterality of acute intracerebral haemorrhage (ICH) and poor clinical outcomes.

148 ticoagulants (NOAC)-associated intracerebral haemorrhage (ICH) are largely unknown.

149 mined injury progression after intracerebral haemorrhage (ICH) induced by collagenase in mice using a

150 ure (BP) at the acute phase of intracerebral haemorrhage (ICH) is beneficial.

151 Poor prognosis after intracerebral haemorrhage (ICH) is related to haemorrhage characterist

152 Intraventricular extension of intracerebral haemorrhage (ICH) predicts poor outcome, but the signifi

153 Intraventricular extension of intracerebral haemorrhage (ICH) predicts poor outcome, but the signifi

154 ous malformation (AVM)-related intracerebral haemorrhage (ICH) than other AVM or ICH scores.

155 ns (CCMs) can cause symptomatic intracranial haemorrhage (ICH), but the estimated risks are imprecise

156 e a predictor of outcome after intracerebral haemorrhage (ICH).

157 quality of life (HRQoL) after intracerebral haemorrhage (ICH).

158 are harmed by early symptomatic intracranial haemorrhage (ICH).

159 (CAA) is associated with lobar intracerebral haemorrhage (ICH).

160 rm prognosis after spontaneous intracerebral haemorrhage (ICH).

161 quality of life (HRQoL) after intracerebral haemorrhage (ICH).

162 al injury also occurs following subarachnoid haemorrhage in an animal model.

163 oxylase enzyme, presenting with hypertensive haemorrhage in basal ganglia and chronic hypokalemia-med

164 grade 3 or 4 postoperative adverse event was haemorrhage in both groups (8 women [3%] in the primary-

165 fter acute spontaneous primary intracerebral haemorrhage in people taking antiplatelet therapy might

166 may alleviate thrombolytic treatment-induced haemorrhage in stroke victims.

167 examine the absolute risks of intracerebral haemorrhage in the context of functional outcome at 90-1

168 re we studied acute sequelae of subarachnoid haemorrhage in the gyrencephalic brain of propofol-anaes

169 e deemed related to study drug, one cerebral haemorrhage in the lenvatinib plus everolimus group and

170 s (seizure after discharge and intracerebral haemorrhage in the recreational activity group and heart

171 e stroke (ischaemic or primary intracerebral haemorrhage) in England and Wales between April 1, 2013,

172 one grade 1 treatment-related event (vaginal haemorrhage, in a patient treated with standard chemothe

173 higher in patients with lobar intracerebral haemorrhage (incidence at 1 year 23.4%, 14.6-33.3) than

174 an for patients with non-lobar intracerebral haemorrhage (incidence at 1 year 9.2%, 5.1-14.7).

175 00-380,000) cases with fever and jaundice or haemorrhage including 78,000 (95% CI 19,000-180,000) dea

176 ut the absolute excess risk of intracerebral haemorrhage increased with increasing stroke severity: f

177 xclusion criteria were pure intraventricular haemorrhage; intracerebral haemorrhage resulting from in

178 outcomes included antepartum or intrapartum haemorrhage, intrapartum fever, postpartum treatment wit

179 Haemorrhage is a common cause of death in trauma patient

180 Intraventricular haemorrhage is a subtype of intracerebral haemorrhage, w

181 these processes in spontaneous intracranial haemorrhage is poorly understood.

182 patients with acute aneurysmal subarachnoid haemorrhage is unclear.

183 ses as long as the cause of gastrointestinal haemorrhage is unidentified.

184 s, with dIVH defined as new intraventricular haemorrhage (IVH) on the latter scan.

185 e volume (IVH) with/without intraventricular haemorrhage (IVH) over 24 h were estimated in analyses o

186 Two patients died: one had a haemorrhage (judged related to study treatment), and one

187 d: CNS involvement, a stroke or intracranial haemorrhage less than 12 months before enrolment, clinic

188 ubgroup analysis, according to intracerebral haemorrhage location.

189 33 patients had a recurrent subarachnoid haemorrhage more than 1 year after their initial haemorr

190 s of alteplase on the risks of intracerebral haemorrhage, mortality, and functional impairment in dif

191 = 11) or were made anaemic by isovolumetric haemorrhage (n = 12) for 1 week prior to myocardial cont

192 ia (n=2), pneumonia aspiration (n=1), rectal haemorrhage (n=1), dyspnoea (n=1), failure to thrive (n=

193 (n=1), and in the placebo group were a brain haemorrhage (n=1), myocardial infarction (n=1), and gast

194 outnumbered disabling or fatal intracerebral haemorrhage (n=45 vs n=18), with an absolute risk of 9.1

195 Perioperative haemorrhage negatively affects patient outcomes and resu

196 arrest, pneumonia, sepsis, and subarachnoid haemorrhage), none were deemed treatment related.

197 age volume less than 30 mL, intraventricular haemorrhage obstructing the 3rd or 4th ventricles, and n

198 Late seizures after intracerebral haemorrhage occur after the initial acute haemorrhagic i

199 symptomatic post-thrombolysis intracerebral haemorrhages occurred in 28 of 675 patients (4.1%, 95% C

200 ase increased the odds of type 2 parenchymal haemorrhage (occurring in 231 [6.8%] of 3391 patients al

201 more likely to have pseudoexfoliation, disc haemorrhages, ocular medication changes, and IOP-lowerin

202 a non-traumatic (spontaneous) intracerebral haemorrhage of 20 mL or higher to standard medical care

203 3 patients vs five [3%] of 184 patients) and haemorrhage of any type (17 [4%] of 403 vs one [<1%] of

204 Haemorrhage of grade 3 or higher was reported in ten (16

205 rial, to model the log odds of intracerebral haemorrhage on allocation to alteplase, treatment delay,

206 nts aged 18 years and older with parenchymal haemorrhage on the first CT scan.

207 anges to the small vessels) instead of frank haemorrhages on histology.

208 etroperitoneal haemorrhage, one subarachnoid haemorrhage, one respiratory distress, and one from dise

209 unrelated to treatment (one retroperitoneal haemorrhage, one subarachnoid haemorrhage, one respirato

210 the syndrome is complicated by intracranial haemorrhage or brain infarction.

211 CAA versus patients with deep intracerebral haemorrhage or healthy controls.

212 n mortality, most often as a result of acute haemorrhage or massive posterior fossa oedema causing ob

213 failure of aneurysm treatment, intracranial haemorrhage or residual aneurysm on 1-year imaging.

214 osite outcome (death, non-fatal intracranial haemorrhage, or new/worse persistent focal neurological

215 ith headache, ischaemic stroke, subarachnoid haemorrhage, or symptoms associated with mass effect, mo

216 -free survivors of spontaneous intracerebral haemorrhage; our results suggest that underlying cerebra

217 PMCTA was better at identifying trauma and haemorrhage (p=0.008), whereas autopsy was better at ide

218 Deaths from post-partum haemorrhage peaked 2-3 h after childbirth.

219 ulmonary dysplasia, sepsis, intraventricular haemorrhage, periventricular leukomalacia, and necrotisi

220 morrhagic infarction and 26 were parenchymal haemorrhage (PH).

221 morrhage from the Prognosis of Intracerebral Haemorrhage (PITCH) cohort who were admitted to Lille Un

222 lated to sunitinib], one oesophageal varices haemorrhage [possibly related to sunitinib], one cardiac

223 : loss of >/=5 letters of visual acuity, new haemorrhage, presence of IRF and SRF on an optical coher

224 tionally significant feature of subarachnoid haemorrhage, raising the prospect of common diagnostic,

225 ck-box warned serious SEs, namely pneumonia, haemorrhage rectum, and retinal bleeding, contributed mo

226 survivors for association with intracerebral haemorrhage recurrence.

227 y in the days and weeks before intracerebral haemorrhage (regression p<0.0001) but not before ischaem

228 s a major cause of mortality in intracranial haemorrhage related to vitamin K antagonists (VKA-ICH).

229 vour the use of PCC over FFP in intracranial haemorrhage related to VKA.

230 ble uterotonics for management of postpartum haemorrhage remains limited in Senegal outside health fa

231 eater frequency of complete intraventricular haemorrhage removal via alteplase produces gains in func

232 The presence of haemorrhage, restricted diffusion, contrast enhancement,

233 intraventricular haemorrhage; intracerebral haemorrhage resulting from intracranial vascular malform

234 1.07, P = 0.04) and recurrent intracerebral haemorrhage risk (hazards ratio, 1.45, P = 0.006).

235 e associated with both primary intracerebral haemorrhage risk (odds ratio, 1.07, P = 0.04) and recurr

236 ad higher risks of antepartum or intrapartum haemorrhage (RR 0.6, 95% CI 0.4-0.9), intrapartum fever

237 t point increase in patients presenting with haemorrhage (RR 0.98, 95% CI 0.96 to 1.00).

238 s of periprocedural symptomatic intracranial haemorrhage (RR=0.59, 95% CI 0.43 to 0.81; p=0.001) and

239 ient ischaemic attack (TIA) and subarachnoid haemorrhage (SAH).

240 sion (HTN) is a risk factor for subarachnoid haemorrhage (SAH).

241 ratification variables and the Intracerebral Haemorrhage Score.

242 In patients with intracerebral haemorrhage seen within 90 min, the highest systolic blo

243 fracture, thrombocytopenia with subcutaneous haemorrhage, severe anaemia, and cardiogenic syncope).

244 , a particularly deadly form of intracranial haemorrhage, shares key pathophysiological features with

245 trials including patients with intracerebral haemorrhage should assess cognitive endpoints.

246 we conclude that patients with subarachnoid haemorrhage should not be treated routinely with simvast

247 acebo; frequency of symptomatic intracranial haemorrhage (six [3%] patients in the desmoteplase group

248 eight [4%]), pneumonia (seven [3%]), gastric haemorrhage (six [3%]), and gastrointestinal haemorrhage

249 found after adjustment for intraventricular haemorrhage size and thalamic intracerebral haemorrhage.

250 nt mottling, depigmentation area, subretinal haemorrhage, subretinal fluid, macula thickness, macular

251 spective cohort of 174 primary intracerebral haemorrhage survivors for association with intracerebral

252 dinal follow-up of consecutive intracerebral haemorrhage survivors presenting to a single tertiary ca

253 s within 6 h of supratentorial intracerebral haemorrhage symptom onset if they had used antiplatelet

254 l oedema (five [2%] vs four [2%]), and major haemorrhage (ten [4%] vs 15 [6%]) was much the same betw

255 is seems worse in patients with subarachnoid haemorrhage than in those without.

256 in the placebo group with severe post-partum haemorrhage than those in the cholecalciferol group (96

257 nsion was more associated with intracerebral haemorrhage than with ischaemic stroke, whereas current

258 of dementia after spontaneous intracerebral haemorrhage that accounts for about 15% of all strokes h

259 One patient died from an intracranial haemorrhage that was judged by the investigator to be du

260 stroke severity: for SITS-MOST intracerebral haemorrhage the absolute excess risk ranged from 1.5% (0

261 e Blood Pressure Reduction in Acute Cerebral Haemorrhage Trials (INTERACT 1 and 2).

262 e Blood Pressure Reduction in Acute Cerebral Haemorrhage Trials (INTERACT 1 and 2).

263 e Blood Pressure Reduction in Acute Cerebral Haemorrhage Trials (INTERACT1 and 2).

264 creased the odds of symptomatic intracranial haemorrhage (type 2 parenchymal haemorrhage definition 2

265 nt of three classifications of intracerebral haemorrhage: type 2 parenchymal haemorrhage within 7 day

266 Most patients with subarachnoid haemorrhage undergo surgical or endovascular treatment t

267 ND) without brain imaging evidence of recent haemorrhage versus other modes of presentation (hazard r

268 (2) of increased haematoma+intraventricular haemorrhage volume (IVH) with/without intraventricular h

269 There was excellent agreement for haemorrhage volume (n=193): ABC/2 intraobserver intracla

270 nit with stable, non-traumatic intracerebral haemorrhage volume less than 30 mL, intraventricular hae

271 Fully automated measurement of haemorrhage volume was possible in only 5% of cases.

272 Postpartum haemorrhage was diagnosed in one woman allocated to oxyt

273 The rate of fetomaternal haemorrhage was higher with the intervention (10.5% in t

274 pressure reading after primary intracerebral haemorrhage was more likely than after ischaemic stroke

275 , the proportional increase in intracerebral haemorrhage was similar irrespective of treatment delay,

276 systolic blood pressure after intracerebral haemorrhage was substantially higher than premorbid leve

277 ase also increases the risk of intracerebral haemorrhage; we aimed to determine the proportional and

278 methods; shape, density and intraventricular haemorrhage were also assessed.

279 e with frontal infarcts and/or intracerebral haemorrhage were both significantly more likely to have

280 A total of 872 survivors of intracerebral haemorrhage were enrolled and followed for a median of 3

281 of misoprostol for prevention of postpartum haemorrhage were excluded to prevent contamination.

282 tients with alcoholic cirrhosis and variceal haemorrhage were studied prior to and 1-hour after TIPSS

283 Asymptomatic haemorrhages were more common in the MIS plus alteplase

284 ons of this particular sample, no additional haemorrhages were observed that were missed on magnetic

285 h usual premorbid levels after intracerebral haemorrhage, whereas acute-phase systolic blood pressure

286 emorrhage within 24-36 h (type 2 parenchymal haemorrhage with a deterioration of at least 4 points on

287 hether attempting to remove intraventricular haemorrhage with alteplase versus saline irrigation impr

288 Hereditary cerebral haemorrhage with amyloidosis-Dutch type (HCHWA-D) is a g

289 othesis in patients with hereditary cerebral haemorrhage with amyloidosis-Dutch type (HCHWA-D), a mon

290 ral basal ganglia bleeding with subarachnoid haemorrhage with no aetiology is uncommon.

291 ociation between CAA and lobar intracerebral haemorrhage (with its high recurrence risk) is now well

292 ar haemorrhage is a subtype of intracerebral haemorrhage, with 50% mortality and serious disability f

293 ion with a high risk of future intracerebral haemorrhage, with potential implications for antithrombo

294 sis in Stroke Monitoring Study's (SITS-MOST) haemorrhage within 24-36 h (type 2 parenchymal haemorrha

295 e SITS-MOST definition of parenchymal type 2 haemorrhage within 36 h), fatal intracranial haemorrhage

296 1-10.84, p<0.0001) and of fatal intracranial haemorrhage within 7 days (91 [2.7%] vs 13 [0.4%]; OR 7.

297 l haemorrhage (defined by type 2 parenchymal haemorrhage within 7 days and, separately, by the SITS-M

298 haemorrhage within 36 h), fatal intracranial haemorrhage within 7 days, and 90-day mortality.

299 roke Scale [NIHSS]); and fatal intracerebral haemorrhage within 7 days.

300 ntracerebral haemorrhage: type 2 parenchymal haemorrhage within 7 days; Safe Implementation of Thromb