ライフサイエンスコーパス: hematoma

1 resulting in hoarse voice (upper esophageal hematoma).

2 cond surgery (screw malposition and epidural hematoma).

3 entation, edema, telangiectatic matting, and hematomas).

4 24 hours and occurrence of large parenchymal hematoma.

5 eavage of the arterial wall by an intramural hematoma.

6 teoblastic cells located at the hedge of the hematoma.

7 A CT scan of his head revealed a subdural hematoma.

8 luding small amounts of adjacent soft tissue hematoma.

9 without the risk of hypotension or epidural hematoma.

10 ded myocardial infarction, nerve injury, and hematoma.

11 ence of clinically significant device-pocket hematoma.

12 ed with pericardial effusions and periaortic hematoma.

13 were associated with higher risk of subdural hematoma.

14 cal complications of cranial nerve palsy and hematoma.

15 as a biconvex, high-attenuating, extraaxial hematoma.

16 failure occurs in patients with subcapsular hematoma.

17 ion, and differing subjective definitions of hematoma.

18 ereas heparin-treated mice had 3-fold larger hematomas.

19 h neoplastic disease than with infections or hematomas.

20 .5% to 5.5% (P<0.001), because of more groin hematomas.

21 %), nasopharyngitis (1%), and injection site hematoma (1%).

22 ions (3.6%), pneumonia (2.3%), hemorrhage or hematoma (1.4%), or pulmonary embolism (0.6%).

23 l or full necrosis (20.1%), and bleeding and hematoma (15.4%).

24 aortic dissection, 35 had intramural aortic hematoma, 18 had aortic rupture, and 10 had penetrating

25 alteplase, 2; P=0.018) and less parenchymal hematoma (2 of 75 versus 10 of 71; P=0.02).

26 of patients were hematuria (2%) and subdural hematoma (2%).

27 rative scarring (0.9 mm(2)/sec +/- 0.00) and hematomas (2.34 mm(2)/sec +/- 0.72) (P = .03 for both).

28 sm, active bleeding, parenchymal injury, and hematoma; 20 cases were interpreted by all radiologists.

29 62.8%), perforation (31.3%), and access-site hematoma (22.9%) were the most frequent modes of present

30 ubarachnoid hemorrhage (33.4%), 134 subdural hematoma (35.0%), and 121 intraparenchymal hemorrhage (3

31 ges acts as an important factor in promoting hematoma absorption and protecting other brain cells fro

32 % were male patients, and 62.6% had subdural hematoma; admission Glasgow Coma Scale score was 3 +/- 1

33 Phagocytosis is necessary to eliminate the hematoma after intracerebral hemorrhage (ICH); however,

34 s, extraconal hematoma, intraconal hematoma, hematoma along the optic nerve, hematoma along the poste

35 ratio, 4.45; 95% CI: 1.91, 10.35; P = .001), hematoma along the posterior globe (odds ratio, 0.326; 9

36 al hematoma, hematoma along the optic nerve, hematoma along the posterior globe, optic canal fracture

37 The intramural duodenal hematoma and critical condition resolved spontaneously a

38 pixaban who developed a spontaneous subdural hematoma and declining mental status that improved after

39 moral neuropathy in one patient, perinephric hematoma and hemobilia in one patient), and one was a si

40 ed factor VII (rFVIIa) reduced growth of the hematoma and improved survival and functional outcomes.

41 arget to bone fracture sites associated with hematoma and inflammation.

42 the sonographic diagnosis of left testicular hematoma and of the right cryptorchidism.

43 iant forms' of aortic dissection: intramural hematoma and penetrating aortic ulcer.

44 cits and were more likely to have periaortic hematoma and pericardial effusion.

45 t blood transfusions, whereas isolated large hematomas and CABG-related bleeding were not significant

46 Access site hematomas and pseudoaneurysms are the most frequent comp

47 stent esophageal dysmotility (mid esophageal hematoma), and vocal cord paralysis, resulting in hoarse

48 s, increase sensitivity (especially for thin hematomas), and reduce the required operator experience

49 l ischemia at baseline remote from the index hematoma, and (1/4) of patients experience ongoing, acut

50 include avoiding cranial nerve damage, wound hematoma, and general anesthesia.

51 y, organ malperfusion, increasing periaortic hematoma, and hemorrhagic pleural effusion on imaging id

52 ysmal subarachnoid hemorrhage, intracerebral hematoma, and trauma.

53 ruptio placentae, renal failure, subcapsular hematomas, and hepatic rupture.

54 eoplastic epidural disease: Six patients had hematomas, and nine had abscesses.

55 was associated with higher risk of subdural hematoma; and the highest odds of subdural hematoma was

56 hift, depressed skull fracture, and epidural hematoma are key risk factors for needing intensive care

57 uch as intracystic, subdural, and extradural hematomas are well known after a trauma, spontaneous hem

58 factors following surgery for acute subdural hematomas (ASDHs) in England and Wales over a 20-year pe

59 served on the neurovascular structure around hematoma at 24 hrs after ICH, along with perivascular as

60 ty, intracranial hemorrhage, and parenchymal hematoma at 90 days were also assessed.

61 and apposition, but also residual intramural hematoma at the stented site (abluminal) and at the dist

62 induction, animals demonstrate reproducible hematomas, brain edema formation and marked neurological

63 gned to stabilize hematoma growth and reduce hematoma burden may improve outcomes.

64 ic therapy with rFVIIa reduced growth of the hematoma but did not improve survival or functional outc

65 The identification of hematomas (by these imaging devices) in the mediastinum

66 nt therapy, use of drains, irrigation of the hematoma cavity, bed rest, and treatment of recurrences

67 nstrated that MDMs are essential for optimal hematoma clearance and neurological recovery.

68 istration results in reduced edema, enhanced hematoma clearance, and improved neurological outcomes i

69 efferocytosis of eryptotic erythrocytes and hematoma clearance, worsened neurological recovery, exac

70 among those >80 yrs of age (36% of subdural hematoma cohort), in lower income patients, in patients

71 tive complications following PAN, hemorrhage/hematoma complications following PCI, and septicemia fol

72 CT showed a voluminous subcapsular hematoma compressing the hepatic parenchyma, which appea

73 le the principal controversy over intramural hematoma concerns its management when the ascending aort

74 of surgical management of type A intramural hematoma continues to mount, although it is also clear t

75 e incidence of clinically significant pocket hematoma (CSH).

76 Neurosurgical intervention for subdural hematoma decreased from 41% in 1998 to 31% in 2007 (p <

77 For all readers, reading time for hematoma detection was significantly shorter (3-5 times

78 Empiric antibiotics upon development of hematoma did not reduce long-term infection risk.

79 the response to clear iron released from the hematoma during clot resolution.

80 t 4 hours was associated with lower rates of hematoma enlargement (35/193 [18.1%] vs 220/498 [44.2%]

81 Frequency of hematoma enlargement in relation to international normal

82 Reduced rates of hematoma enlargement were associated with reversal of IN

83 term functional outcome, 853 for analysis of hematoma enlargement, and 719 for analysis of OAC resump

84 4 hours were associated with lower rates of hematoma enlargement, and resumption of OAC therapy was

85 Because the hematoma entirely replaced the normal parenchyma, orchie

86 y with a motor system power of grade 4 after hematoma evacuation and treatment with antibiotics, anti

87 Subdural hematoma evacuation was associated with decreased mortal

88 agulation therapy, or further surgery (e.g., hematoma evacuation).

89 , hypoxemia, acidosis, tobacco use, emergent hematoma evacuation, and vasopressor dependence.

90 ed brain biopsy specimen, biopsy specimen at hematoma evacuation, or autopsy) and available brain MRI

91 nificant (>33%) expansion; 2 required urgent hematoma evacuation.

92 ecimens, and 31 with pathologic samples from hematoma evacuations.

93 ients should be observed postoperatively for hematoma, evaluated for hypocalcemia and symptoms of hyp

94 Primary outcome was substantial hematoma expansion (>33% or >6 mL) at 24 hours.

95 The association between hypodensities and hematoma expansion (>6 cm3 or 33% of baseline volume) wa

96 icant effect on the frequency of substantial hematoma expansion (43% [12 of 28] for prothrombin compl

97 analyses, hypodensities were associated with hematoma expansion (86 of 163 patients with hematoma exp

98 t 2 points, and the frequency of substantial hematoma expansion (defined as relative [>/= 33%] or abs

99 rmed well and showed strong association with hematoma expansion (odds ratio, 4.59; P < .001 for a hig

100 sign in any phase was related to substantial hematoma expansion (P < .001 for all comparisons; Bonfer

101 sion vs in 25.0% (15 of 60) of patients with hematoma expansion (P = .01), highlighting a role for cr

102 on, the greater the frequency of substantial hematoma expansion (P = .013).

103 , the frequency and clinical significance of hematoma expansion after childhood intracerebral hemorrh

104 In patients with sequential imaging for the hematoma expansion analysis, substantial hematoma expans

105 ated ICH, of whom 45 (74%) qualified for the hematoma expansion analysis.

106 reverse coagulopathy early enough to prevent hematoma expansion and improve the outcome of thrombolys

107 and whether intensive BP reduction decreases hematoma expansion and improves outcome in patients with

108 should include strategies designed to reduce hematoma expansion and limit the medical consequences of

109 The effect of hyperglycemia on hematoma expansion and PK-mediated inhibition of platele

110 Hyperglycemia is associated with greater hematoma expansion and poor clinical outcomes after intr

111 vel marker may help clarify the mechanism of hematoma expansion and serve as a useful addition to cli

112 nts with ICH who are likeliest to experience hematoma expansion and therefore likeliest to benefit fr

113 has been implicated in contributing to both hematoma expansion and thrombosis in stroke, its role in

114 CT) scans within 48 hours were evaluated for hematoma expansion and were compared with children with

115 suggest that hyperglycemia augments cerebral hematoma expansion by PK-mediated osmotic-sensitive inhi

116 Many clinical trials focus on restricting hematoma expansion following acute intracerebral hemorrh

117 rucizumab in equimolar dose prevented excess hematoma expansion for both DE doses.

118 [52.8%], whereas 136 of 621 patients without hematoma expansion had hypodensities [21.9%]; P < .001).

119 hematoma expansion (86 of 163 patients with hematoma expansion had hypodensities [52.8%], whereas 13

120 acerebral injection of purified PK augmented hematoma expansion in both diabetic and acutely hypergly

121 independently associated with more frequent hematoma expansion in patients with lobar ICH.

122 , 1.04-1.99; P = .03; respectively) and with hematoma expansion in the lobar ICH group (odds ratio, 1

123 trolling for other variables associated with hematoma expansion in univariate analyses with P </= .10

124 Hematoma expansion is a potentially modifiable predictor

125 Importance: Hematoma expansion is an important determinant of outcom

126 selecting those patients at highest risk of hematoma expansion is challenging.

127 gh mortality and an unfavorable outcome, and hematoma expansion is frequent.

128 Hematoma expansion is the only modifiable predictor of o

129 Hematoma expansion occurred in 156 patients (19.1%).

130 the hematoma expansion analysis, substantial hematoma expansion occurred in 38% (17 of 45).

131 Hematoma expansion occurred in 7 of 22 (32%).

132 Hematoma expansion occurs in children with intracerebral

133 The association between hypodensities and hematoma expansion remained significant (odds ratio, 3.4

134 The incidence of hematoma expansion steadily increased with higher scores

135 We show that cerebral hematoma expansion triggered by intracerebral infusion o

136 Covariates were tested for association with hematoma expansion using univariate and multivariable lo

137 rring in 36.3% (8 of 22) of patients without hematoma expansion vs in 25.0% (15 of 60) of patients wi

138 Hematoma expansion was assessed using semiautomated soft

139 neous ICH without anticoagulant therapy, and hematoma expansion was calculated.

140 Hematoma expansion was defined as an increase of more th

141 A 9-point prediction score for hematoma expansion was developed and independently valid

142 e putative effect of laropiprant on limiting hematoma expansion was tested by an in vivo tail bleedin

143 iable model; other independent predictors of hematoma expansion were a CT angiography spot sign, a sh

144 he presence of the spot sign and substantial hematoma expansion were assessed by using the Pearson ch

145 in ICH aimed at patients at highest risk of hematoma expansion with maximum potential for therapeuti

146 tal mortality, and the secondary outcome was hematoma expansion, defined as a 33% increase in the hem

147 ute ICH detected on an NCCT scan may predict hematoma expansion, independent of other clinical and im

148 Hematoma expansion, intraventricular hemorrhage, and rev

149 For this planned substudy of hematoma expansion, neonates 28 days or younger and part

150 total mortality rates, unfavorable outcomes, hematoma expansion, neurologic deterioration, and severe

151 nogen level, <150 mg/dL) was associated with hematoma expansion, occurring in 36.3% (8 of 22) of pati

152 these SVD markers and ICH volume, as well as hematoma expansion, were investigated using multivariabl

153 the risk of and treatment stratification for hematoma expansion.

154 (NCCT) have been suggested as a predictor of hematoma expansion.

155 amework for future studies aimed at limiting hematoma expansion.

156 52.3% (67 of 128), and 26.8% (22 of 82) had hematoma expansion.

157 e the likelihood of in-hospital mortality or hematoma expansion.

158 within 48 hours that could be evaluated for hematoma expansion.

159 Primary outcome was prevalence of hematoma expansion.

160 n and can help stratify patients at risk for hematoma expansion.

161 ured by baseline hematoma volume and risk of hematoma expansion.

162 such as brain trauma, localized brain edema, hematoma, focal cerebral ischemia, or brain tumors.

163 , idarucizumab prevents excess intracerebral hematoma formation in mice anticoagulated with dabigatra

164 is thought to occur secondary to mesenteric hematoma formation or mesenteric tear complications.

165 vertent arterial puncture, pneumothorax, and hematoma formation.

166 The increased incidence of subdural hematoma from 2000 to 2015 appears to be associated with

167 res differentiate presentation of esophageal hematoma from that of an atrio-esophageal fistula.

168 Absolute hematoma growth analysis revealed a hierarchical pattern

169 New therapies designed to stabilize hematoma growth and reduce hematoma burden may improve o

170 Expansion of ICH was defined as hematoma growth of greater than 33%, and an unfavorable

171 have shown that early hemostasis to prevent hematoma growth, removal of clot by surgical or minimall

172 Incidence of subdural hematoma has been reported to be increasing.

173 The prevalence and total cost for subdural hematoma has increased significantly in the last decade

174 Intraoperatively, an extratesticular hematoma, hematocele, and rupture were confirmed but tor

175 l fractures, extraconal hematoma, intraconal hematoma, hematoma along the optic nerve, hematoma along

176 lications (pericardial effusion, pericardial hematoma, hemoperitoneum, and pericardial tamponade).

177 oedema, presence of subdural and extradural hematoma; however in isolation there was no statistical

178 Intramural duodenal hematoma (IDH) rarely occurs after endoscopic interventi

179 A double-lumen or intramural hematoma image was visualized in all cases.

180 Acute aortic intramural hematoma (IMH) is an important subgroup of aortic dissec

181 Management of acute type A intramural hematoma (IMH) remains controversial, varying from immed

182 been described in >20% of type B intramural hematomas (IMH), with unclear prognosis and management.

183 was identified in 20 patients and periaortic hematoma in 11.

184 Cervical artery dissection (CeAD), a mural hematoma in a carotid or vertebral artery, is a major ca

185 nce standard helped confirm 121 intracranial hematomas in 39 patients.

186 so showed more protein leakage and developed hematomas in the Matrigel model.

187 matoma risk and determine trends in subdural hematoma incidence and antithrombotic drug use in the ge

188 Subdural hematoma incidence and antithrombotic drug use was ident

189 The overall subdural hematoma incidence rate increased from 10.9 per 100000 p

190 atoma with antithrombotic drug use, subdural hematoma incidence rate, and annual prevalence of treatm

191 ular complications (consisting of hemorrhage/hematoma, incidents requiring surgical repair, and accid

192 ten detection time for epidural and subdural hematomas, increase sensitivity (especially for thin hem

193 Hospitalizations for subdural hematoma increased from 59,373 (30 per 100,000 hospitali

194 The prevalence of subdural hematoma increased with age (p < .001), particularly amo

195 Rates of hematoma, infection, urinary retention, and recurrence w

196 e evaluated: midfacial fractures, extraconal hematoma, intraconal hematoma, hematoma along the optic

197 MRI revealed a consistent hematoma involving the striatum and overlying corpus cal

198 g iron-scavenging lactoferrin that may limit hematoma/iron-mediated brain injury after intracerebral

199 Subdural hematoma is a common type of intracranial hemorrhage, pa

200 Esophageal hematoma is a rare but important differential diagnosis

201 An idiopathic scrotal hematoma is a very rare condition that can simulate it.

202 Health resource consumption for subdural hematoma is increasing without clear evidence that manag

203 Hematomas less than 3 mm thick were considered thin.

204 eal fistula and was diagnostic of esophageal hematoma localized to either the upper esophagus or exte

205 ion and outcome following ICH, regardless of hematoma location.

206 Strategies aimed at reducing hematomas may decrease the long-term risk of infection.

207 ns should recognize that patients with large hematomas may make a substantial recovery.

208 (approximately 90% of cases) and intramural hematoma, may be complicated by poor perfusion, aneurysm

209 Among 10010 patients with subdural hematoma (mean age, 69.2 years; 3462 women [34.6%]), 47.

210 penetrating aortic ulcer (n = 6), intramural hematoma (n = 2), and mycotic aneurysm (n = 2).

211 Complications associated with surgery were hematoma (n = 5, conservative treatment), infection (ant

212 .9 +/- 2.1 mm(2)), the associated intramural hematoma (n = 9), and thrombi in the true or false lumen

213 Clinically significant device-pocket hematoma occurred in 12 of 343 patients (3.5%) in the co

214 Subdural hematoma occurred in 8 patients (2 in the core study, 6

215 No sICH or parenchymal hematomas occurred.

216 h significance as predictors were intraconal hematoma (odds ratio, 12.73; 95% confidence interval [CI

217 CI: 0.111, 0.958; P = .041), and extraconal hematoma (odds ratio, 2.36; 95% CI: 1.03, 5.41; P = .042

218 atient did not have any mesenteric injury or hematoma on initial abdominal CT.

219 ebral hemorrhage, pericardial complications, hematoma or hemorrhage, blood transfusion, or cardiogeni

220 bleeding (OR, 0.39; 95% CI, 0.27-0.57), and hematoma (OR, 0.36; 95% CI, 0.27-0.48) compared with fem

221 upted warfarin therapy groups in access site hematoma (OR, 0.59; 95% confidence interval [CI]: 0.33,

222 as associated with lower odds of access site hematoma (OR, 0.68; 95% CI: 0.51, 0.91; P = .01), bleedi

223 as associated with lower odds of access site hematoma (OR, 0.70; 95% CI: 0.50, 0.99; P = .04), any bl

224 43; 95% CI, 2.88-18.98; P=0.001), periaortic hematoma (OR, 3.06; 95% CI, 1.38-6.78; P=0.006), descend

225 re (OR, 6.5; 95% CI, 3.7-11.4), and epidural hematoma (OR, 3.4; 95% CI, 1.8-6.2).

226 e evaluated, VCDs were associated with fewer hematomas (OR, 0.69 [CI, 0.58 to 0.83]; P < 0.001) or ps

227 al hemorrhage, ischemic stroke, sub/epidural hematoma, or cerebral thrombophlebitis was identified as

228 efined as any transfusion, any hemorrhage or hematoma, or the need for percutaneous or surgical inter

229 sition, length of stay, and cost of subdural hematoma over time.

230 Parenchymal hematoma (PH) following intravenous thrombolysis (IVT) i

231 Parenchymal hematoma (PH) was defined using European Cooperative Acu

232 ed 20 to 89 years with a first-ever subdural hematoma principal discharge diagnosis from 2000 to 2015

233 The hematoma produced in this model was primarily restricted

234 nation revealed marked periorbital edema and hematoma, ptosis, ocular movements limitation, an infero

235 Esophageal hematoma recently has been reported as a form of esophag

236 er outcomes such as surgical site infection, hematoma, reintervention, or readmission.

237 CSH was defined as a post-procedure hematoma requiring further surgery and/or resulting in p

238 for pocket exploration or blood transfusion; hematoma requiring pressure dressing or change in antico

239 significantly lower incidence of bleeding or hematoma requiring red blood cell transfusions (0.9% ver

240 both groups (1 tamponade in RivG and 1 groin hematoma requiring transfusion in phenprocoumon).

241 used to model ICH and to study mechanisms of hematoma resolution and phagocytosis regulation by perox

242 e PPARgamma agonist, rosiglitazone, promoted hematoma resolution, decreased neuronal damage, and impr

243 mposite of access-site bleeding, access-site hematoma, retroperitoneal bleeding, or any vascular comp

244 genesis, as well as reduced apoptosis in the hematoma rim compared to the corresponding control group

245 een use of antithrombotic drugs and subdural hematoma risk and determine trends in subdural hematoma

246 0.00; 95% CI, -0.02 to 0.03) or parenchymal hematoma (RR, 1.18; 95% CI, 0.71-1.94; RD, 0.01; 95% CI,

247 Peripancreatic fluid collections include hematoma/seroma, pseudocyst, and abscess.

248 report, we suggest that intramural duodenal hematoma should be considered if a patient has the tetra

249 Larger hematoma size (hazard ratio [HR], 1.47 per 10-mL increas

250 early after ICH is strongly associated with hematoma size and location.

251 f spleen shrinkage was associated with brain hematoma size, and a reduced progression of perihematoma

252 ICH but does not affect MRI or histological hematoma size.

253 ng that may represent dissection, intramural hematoma, spasm, or tortuosity.

254 as testicular rupture, dislocation, torsion, hematoma, spermatic cord injury or contusion, and epidid

255 Minor bleeding was defined as hematoma that did not require intervention.

256 hematoma, which was defined as device-pocket hematoma that necessitated prolonged hospitalization, in

257 ing was defined as either cardiac tamponade, hematoma that required intervention, or bleeding that re

258 For thin hematomas, the mean detection rate increased from 20% (e

259 ith larger basal maximum aortic diameter and hematoma thickness.

260 defined as a bleeding complication including hematoma, transfusion, or prolonged hospital stay.

261 lacement, three of five were associated with hematomas, two of five migrated without identifiable cau

262 atment patients (7%) developed a parenchymal hematoma type 2 (P > .99).

263 dy (SITS-MOST), which included a parenchymal hematoma type 2 and at least a 4-point increase in the N

264 Arteriography and evacuation of the hematoma under ultrasound guidance (while managing hemod

265 k, vascular access complications (hemorrhage/hematoma, vascular complications requiring surgical repa

266 ons between serum calcium level and baseline hematoma volume and between serum calcium level and ICH

267 Pretreatment with DE increased intracerebral hematoma volume and cerebral hemoglobin content.

268 ges on Neuroimaging [STRIVE] guidelines) and hematoma volume and expansion in patients with lobar or

269 in patients with ICH as measured by baseline hematoma volume and risk of hematoma expansion.

270 after intracerebral hemorrhage, brain edema, hematoma volume and the number of apoptotic cells were q

271 mes (p<0.001) but overestimated histological hematoma volume by approximately 5-fold.

272 Furthermore, cisternal hematoma volume correlated with HO-1 activity and cytoki

273 Hematoma volume is the strongest predictor of outcome in

274 in this cohort were small, with a mean (SD) hematoma volume of 17 (9.9) mL, and were subcortical in

275 expansion, defined as a 33% increase in the hematoma volume on follow-up imaging.

276 Predictors of hematoma volume only partially overlap between deep and

277 sity volumes were not associated with either hematoma volume or expansion.

278 lcemic patients had a higher median baseline hematoma volume than did normocalcemic patients (37 mL [

279 The mean (SD) baseline hematoma volume was 23.7 (31.3) mL.

280 effect of intrastriatal infusion of blood on hematoma volume, neurologic function, brain edema and sw

281 on specificity of factors reported to affect hematoma volume.

282 intraoperative hemorrhage and postoperative hematoma volumes compared to those of vehicle preconditi

283 Baseline and follow-up hematoma volumes, detected by noncontrast computed tomog

284 The procedural incidence of esophageal hematoma was 0.27% (3/1110 procedures, mortality 0%).

285 of permeability abnormality for parenchymal hematoma was 83%.

286 l hematoma; and the highest odds of subdural hematoma was associated with combined use of a VKA and a

287 On US, a large hematoma was detected between the leaves of the tunica v

288 The risk of subdural hematoma was highest when a VKA was used concurrently wi

289 Hematoma was punctured to relieve pressure on hepatic pa

290 Access-site hematoma was the most common complication overall (4.2%)

291 Only 1 adverse event (mild injection site hematoma) was assessed as treatment-related.

292 d in all patients: dissection and intramural hematoma were the most common.

293 ome was clinically significant device-pocket hematoma, which was defined as device-pocket hematoma th

294 Association of subdural hematoma with antithrombotic drug use, subdural hematoma

295 ranial CT scan revealed a worsening subdural hematoma with midline shift, a single dose of factor VII

296 fall with head trauma resulting in subdural hematoma with no associated neurological deficits; this

297 nd spermatic cord that showed a left scrotal hematoma with superior displacement of the didymus; the

298 vious studies have inconsistently associated hematoma with the subsequent development of device infec

299 PLP2(-/-) mice produce significantly smaller hematomas with reduced brain hemoglobin content compared

300 omputed tomography was available to define a hematoma without corroborating evidence of other patholo