ライフサイエンスコーパス: hematoma

1 cond surgery (screw malposition and epidural hematoma).

2 ent-related death was reported (intracranial hematoma).

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

4 wound dehiscence, skin necrosis, seroma, and hematoma.

5 were associated with higher risk of subdural hematoma.

6 failure occurs in patients with subcapsular hematoma.

7 ion, and differing subjective definitions of hematoma.

8 eavage of the arterial wall by an intramural hematoma.

9 teoblastic cells located at the hedge of the hematoma.

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

11 t patients with symptomatic chronic subdural hematoma.

12 luding small amounts of adjacent soft tissue hematoma.

13 without the risk of hypotension or epidural hematoma.

14 ded myocardial infarction, nerve injury, and hematoma.

15 ence of clinically significant device-pocket hematoma.

16 ystemic neuropathy, or nerve entrapment from hematoma.

17 ery is narrowed or occluded by an intramural hematoma.

18 cture, one sternal fracture, and one adrenal hematoma.

19 24 hours and occurrence of large parenchymal hematoma.

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

21 cations were limited to three self-resolving hematomas.

22 ergency treatment of spontaneous soft-tissue hematomas.

23 %), nasopharyngitis (1%), and injection site hematoma (1%).

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

25 ive, 1 after 30 days, both drained), 3 groin hematomas (1 of them due to needing heparin for venous t

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

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

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

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

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

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

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

33 % were male patients, and 62.6% had subdural hematoma; admission Glasgow Coma Scale score was 3 +/- 1

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 Complications, including one case of hematoma and 4 cases of mild hemoptysis, and 30-day mort

38 luate the putative link between intraleaflet hematoma and aortic valve calcification and to assess it

39 The intramural duodenal hematoma and critical condition resolved spontaneously a

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

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

42 two (2.5%) patients, respectively, had renal hematoma and macroscopic hematuria; none required any sp

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

44 Access site hematomas and pseudoaneurysms are the most frequent comp

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

46 t blue dye staining of the conjunctiva, neck hematoma, and suture abscess.

47 ysmal subarachnoid hemorrhage, intracerebral hematoma, and trauma.

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

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

50 Intraleaflet hematomas are associated with advanced stages of aortic

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

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

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

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

55 nd invasion of neutrophils into the fracture hematoma, both seen in the early phase after fracture, a

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

57 toward red blood cells (an in vitro model of hematoma clearance after intracerebral hemorrhage [ICH])

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

59 reduced neurological deficits, and improved hematoma clearance, a function that normally requires mi

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

61 Microglia and macrophages carry out hematoma clearance, thereby facilitating functional reco

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

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

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

65 continuation reduced clinically significant hematomas (CSH) by 80% compared with heparin bridging (3

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

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

68 f whom had undergone surgery to remove their hematomas during the index admission, treatment with dex

69 and 94% underwent surgery to evacuate their hematomas during the index admission; 60% in both groups

70 ed major adverse events; minor puncture site hematomas/edema occurred in 5 of 25 (20%).

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

72 Frequency of hematoma enlargement in relation to international normal

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

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

75 4 hours were associated with lower rates of hematoma enlargement, and resumption of OAC therapy was

76 rihematomal region in the pathophysiology of hematoma enlargement.

77 Because the hematoma entirely replaced the normal parenchyma, orchie

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

79 d groups included 152 patients with surgical hematoma evacuation vs 152 patients with conservative tr

80 After adjustment, surgical hematoma evacuation vs conservative treatment was not si

81 Surgical hematoma evacuation vs conservative treatment.

82 3 was identified; below this level, surgical hematoma evacuation was associated with lower likelihood

83 The association of surgical hematoma evacuation with clinical outcomes in patients w

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

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

86 Among patients with cerebellar ICH, surgical hematoma evacuation, compared with conservative treatmen

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

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

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

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

91 een-group differences of total intracerebral hematoma expansion (%) (median [interquartile range]: 8.

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

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

94 9.2 [20.7]; p = 0.900), and intraventricular hematoma expansion (14.5 [63.2] vs 6.1 [40.4]; p = 0.304

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 Primary outcome was relative hematoma expansion from baseline to follow-up CT.

114 Among patients with hematoma expansion greater than or equal to 33% compared

115 The occurrence of hematoma expansion greater than or equal to 33% was simi

116 [52.8%], whereas 136 of 621 patients without hematoma expansion had hypodensities [21.9%]; P < .001).

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

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

119 , 1.04-1.99; P = .03; respectively) and with hematoma expansion in the lobar ICH group (odds ratio, 1

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

121 Hematoma expansion is a potentially modifiable predictor

122 Importance: Hematoma expansion is an important determinant of outcom

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

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

125 Hematoma expansion is the only modifiable predictor of o

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

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

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

129 Hematoma expansion occurs in children with intracerebral

130 ne vasopressin showed no benefit in limiting hematoma expansion or improving functional outcome.

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

132 The incidence of hematoma expansion steadily increased with higher scores

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

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

135 Hematoma expansion was assessed using semiautomated soft

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

137 Hematoma expansion was defined as an increase of more th

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

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

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

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

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

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

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

145 Hematoma expansion, intraventricular hemorrhage, and rev

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

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

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

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

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

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

152 the risk of and treatment stratification for hematoma expansion.

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

154 amework for future studies aimed at limiting hematoma expansion.

155 52.3% (67 of 128), and 26.8% (22 of 82) had hematoma expansion.

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

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

158 Primary outcome was prevalence of hematoma expansion.

159 iodine markers of extravasation for risk of hematoma expansion.

160 evaluation of the spot sign for intracranial hematoma expansion.

161 In this Danish cohort study, risk of spinal hematoma following lumbar puncture was 0.20% among patie

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

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

164 vertent arterial puncture, pneumothorax, and hematoma formation.

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

166 cerebral hemorrhage patients at high risk of hematoma growth (HG).

167 Absolute hematoma growth analysis revealed a hierarchical pattern

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

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

170 n outcomes in patients with chronic subdural hematoma has not been well studied.

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

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

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

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

175 e concentration in the brightest spot in the hematoma (I(bs)) as predictors of expansion.

176 ation: total iodine concentration within the hematoma (I(h)) and focal iodine concentration in the br

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

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

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

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

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

182 Subdural hematoma incidence and antithrombotic drug use was ident

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

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

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

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

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

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

189 Chronic subdural hematoma is a common neurologic disorder that is especia

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

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

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

193 tact with the senescent RBCs of intraleaflet hematomas may play a critical role in the initiation of

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

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

196 ong adults with symptomatic chronic subdural hematoma, most of whom had undergone surgery to remove t

197 type of injury: complex lesions (intramural hematoma, mucosal laceration) and minor lesions (petechi

198 edure site for longer than 48 hours (n = 5), hematoma (n = 3), progressive fracture despite fixation

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

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

201 Overall, spinal hematoma occurred within 30 days for 99 of 49 526 patien

202 No sICH or parenchymal hematomas occurred.

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

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

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

206 aining, the potential impact of intraleaflet hematomas on phenotypic changes in VICs.

207 n of 39 of 46 (85%; 95% CI: 71%, 94%) of the hematomas on the training set (sensitivity of 79% [11 of

208 and 62 of 70 (89%; 95% CI: 79%, 95%) of the hematomas on the validation set (sensitivity of 71% [10

209 Postprocedural access site hematoma or bleeding was noted in 9 patients.

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

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

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

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

214 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

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

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

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

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

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

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

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

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

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

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

225 he importance of IL-4/STAT6/ST2 signaling in hematoma resolution and functional recovery after ICH.

226 CH hastened STAT6 activation and facilitated hematoma resolution.

227 erifemoral hematomas were used as a model of hematoma resolution.

228 t both AMPK and ATF1 are required for normal hematoma resolution.

229 In vivo, femoral hematomas resolved completely between days 8 and 9 in li

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

231 Intraleaflet hematomas, revealed by iron deposits and RBCs into the f

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

233 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,

234 s of needle injection systems, such as pain, hematoma, scar tissue formation, infection or abscess, p

235 erative surgical site occurrences (including hematoma, seroma, surgical site infection, and wound deh

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

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

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

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

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

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

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

243 for the treatment of spontaneous soft-tissue hematomas (SSTHs) and identify variables predictive of s

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

245 2 patients (1 in each group) developed groin hematoma that resolved without any consequences.

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

247 ith larger basal maximum aortic diameter and hematoma thickness.

248 Parenchymal hematoma triggers a series of reactions leading to prima

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

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

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

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

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

254 SAPS II (P < .001), hematoma volume (P = .01), and retroperitoneal location

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

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

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

258 e (SAPS) II, anticoagulation, embolic agent, hematoma volume and location, serum hemoglobin level, he

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

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

261 ith mortality, RLAS score, and DRS score was hematoma volume at follow-up CT.

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

263 Age, Glasgow Coma Scale, and hematoma volume did not modify the effect of surgery.

264 Hematoma volume is the strongest predictor of outcome in

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

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

267 Predictors of hematoma volume only partially overlap between deep and

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

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

270 S II was 42 +/- 13.2 (range, 18-63) and mean hematoma volume was 1419 cm(3) +/- 788 (range, 251-3492

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

272 II was 19.6 +/- 7.1 (range, 13-31) and mean hematoma volume was 862 cm(3) +/- 618 (range, 238-1887 c

273 Coma, temporal lobe involvement, hematoma volume, and electrographic seizures predicted p

274 < 0.001), independently from blood pressure, hematoma volume, and other confounders.

275 Simplified acute physiology score II, hematoma volume, and retroperitoneal location are predic

276 modifying effect of age, Glasgow Coma Scale, hematoma volume, and timing of surgery with meta-regress

277 on specificity of factors reported to affect hematoma volume.

278 er there are differing associations based on hematoma volume.

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

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

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

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

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

284 The decision to surgically evacuate the hematoma was made by the treating clinician.

285 e data, repeat surgery for recurrence of the hematoma was performed in 6 of 349 patients (1.7%) in th

286 Hematoma was punctured to relieve pressure on hepatic pa

287 ip between calcium deposits and intraleaflet hematomas was analyzed by whole-mount staining of calcif

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

289 xplantation, infection, tissue necrosis, and hematoma were comparable between groups.

290 Independent risk factors for spinal hematoma were male sex (adjusted hazard ratio [HR], 1.72

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

292 Residual hematomas were accompanied by increased macrophage infil

293 Perifemoral hematomas were used as a model of hematoma resolution.

294 numbers of neutrophils in the early fracture hematoma, whereas T lymphocytes and markers for cartilag

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

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

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

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

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

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