1,720,985 research outputs found
Infected pseudoaneurysm after carotid endarterectomy: mismatch between clinical presentation and origin
No full text
Tibial artery elongation or redundancy stretch
No full textPatient 1. A 69-year-old man, who is hyperstensive and a smoker, was found to have kinking or looping of both posterior tibial arteries on a lower limb duplex ultrasonography performed for mild lower limb swelling. (A-C). He gave a history bilateral of ankle sprain during child- hood with no major trauma and requiring no invasive or surgical treat- ment. No connective tissue disorder was detected in his family’s medical history.
Patient 2. A 57-year-old woman with hypertension and hyperlipi- demia and who is also a smoker, underwent a supra-aortic vessels and lower limb duplex ultrasonography upon the request of her treating physi- cian. A coiling of the right anterior tibial artery was detected (D). She had no history of right ankle sprain with no family history of connective tissue disorders or major trauma.
Structural remodeling of blood vessels continuously occurs in response to physical and biochemical stimuli. The structural adapta- tion of the vessel internal diameter and wall thickness caused by the circumferential stretch generated by the blood pressure and the wall shear stress generated by the flow are well known and docu- mented mechanisms. Moreover, axial stretch can also play an impor- tant role in arterial structural changes, so that circumferential, radial, and longitudinal wall adaptations usually occur under increased arte- rial pressure.1 However, the effect of sudden and abrupt arterial elongation or stretching that can lead to dissection or elongation in structurally predisposed arteries is less well known.1
The initial elongation and subsequent proliferation of endothelial cells in response to axial stretch have been well documented in an organ culture system by Lee et al.2 Elastic or collagen arterial components can vary in different arterial beds, and arterial elastin component loss could be responsible for fragmentation of elastomers and progressive vessel lengthening.3
Whereas arterial redundancy is well documented in experimental studies, it is difficult to follow the progressive elongation of arteries in pa- tients, given the long time required to identify such an occurrence. Furthermore, classification and grading of arterial kinking, coiling, or loop- ing have not been performed.
Both patients consented to the publication of images and information included in this article.Patient 1. A 69-year-old man, who is hyperstensive and a smoker, was found to have kinking or looping of both posterior tibial arteries on a lower limb duplex ultrasonography performed for mild lower limb swelling. (A-C). He gave a history bilateral of ankle sprain during child- hood with no major trauma and requiring no invasive or surgical treat- ment. No connective tissue disorder was detected in his family’s medical history.
Patient 2. A 57-year-old woman with hypertension and hyperlipi- demia and who is also a smoker, underwent a supra-aortic vessels and lower limb duplex ultrasonography upon the request of her treating physi- cian. A coiling of the right anterior tibial artery was detected (D). She had no history of right ankle sprain with no family history of connective tissue disorders or major trauma.
Structural remodeling of blood vessels continuously occurs in response to physical and biochemical stimuli. The structural adapta- tion of the vessel internal diameter and wall thickness caused by the circumferential stretch generated by the blood pressure and the wall shear stress generated by the flow are well known and docu- mented mechanisms. Moreover, axial stretch can also play an impor- tant role in arterial structural changes, so that circumferential, radial, and longitudinal wall adaptations usually occur under increased arte- rial pressure.1 However, the effect of sudden and abrupt arterial elongation or stretching that can lead to dissection or elongation in structurally predisposed arteries is less well known.1
The initial elongation and subsequent proliferation of endothelial cells in response to axial stretch have been well documented in an organ culture system by Lee et al.2 Elastic or collagen arterial components can vary in different arterial beds, and arterial elastin component loss could be responsible for fragmentation of elastomers and progressive vessel lengthening.3
Whereas arterial redundancy is well documented in experimental studies, it is difficult to follow the progressive elongation of arteries in pa- tients, given the long time required to identify such an occurrence. Furthermore, classification and grading of arterial kinking, coiling, or loop- ing have not been performed.
Both patients consented to the publication of images and information included in this article
Thrombolysis in carotid-related stroke patients: what about plaque hemorrhage and disruption?
No full textOpen conversion after aortic endograft infection. Caused by colistin-resistant, carbapenemase-producing Klebsiella pneumoniae
Full text linkA 62-year-old man presented with fever, abdominal pain, and malaise 13 months after
emergency endovascular aortic repair. Computed tomographic angiograms showed a
periprosthetic fluid and gas collection, so infection was diagnosed. Open conversion was
performed, involving endograft explantation and in situ aortic reconstruction. Cultures and
the explanted prosthesis were positive for carbapenemase-producing Klebsiella pneumoniae,
resistant to colistin. Because of the sparse data on endograft infections caused
by this pathogen, we placed the patient on an empiric double-carbapenem regimen for
4 weeks. Symptomatic recovery occurred after 21 days. On the 30th day, we deployed
a stent to treat a new pseudoaneurysm. Three years later, the patient had no signs of
persistent or recurrent infection. We think that this is the first report of aortic endograft
infection caused by colistin-resistant, carbapenemase-producing K. pneumoniae.A 62-year-old man presented with fever, abdominal pain, and malaise 13 months after
emergency endovascular aortic repair. Computed tomographic angiograms showed a
periprosthetic fluid and gas collection, so infection was diagnosed. Open conversion was
performed, involving endograft explantation and in situ aortic reconstruction. Cultures and
the explanted prosthesis were positive for carbapenemase-producing Klebsiella pneumoniae,
resistant to colistin. Because of the sparse data on endograft infections caused
by this pathogen, we placed the patient on an empiric double-carbapenem regimen for
4 weeks. Symptomatic recovery occurred after 21 days. On the 30th day, we deployed
a stent to treat a new pseudoaneurysm. Three years later, the patient had no signs of
persistent or recurrent infection. We think that this is the first report of aortic endograft
infection caused by colistin-resistant, carbapenemase-producing K. pneumoniae
Infective etiology affects outcomes of late open conversion after failed endovascular aneurysm repair
No full textPURPOSE:
To retrospectively review all patients undergoing late open conversion (LOC) after endovascular aneurysm repair (EVAR) in order to identify any clinical or technical predictors of poor outcome.
METHODS:
Twenty-six consecutive patients (24 men; mean age 74.7 ± 8.3 years) underwent LOC between June 2006 and April 2013 at our institution. The mean interval from index EVAR to LOC was 40.4 ± 29.2 months (range 5-93 months). The indication for LOC was endoleak in 14 (54%) patients and infection in 12 (46%): 2 (8%) patients with endoleak had a ruptured aneurysm and 6 (23%) patients with infection had a recurrent secondary aortoesophageal fistula (sAEF).
RESULTS:
In all 12 cases of infection and in 12 of 14 endoleaks, the entire endograft was explanted. A rifampin-soaked Dacron silver graft was implanted in all patients with infection. Patients with any infection and with recurrent AEF required more blood units than patients with endoleak (6.40 vs. 1.86, p = 0.045; 6.76 vs. 1.86, p = 0.0036, respectively). Compared with endoleak, the duration of conversions in the setting of infection (274 vs. 316 minutes, p = 0.42) and recurrent sAEF (274 vs. 396 minutes, p = 0.021) was longer. All patients with recurrent sAEF died at a mean 3.0 ± 2.5 days after LOC from proximal anastomosis disruption and hemorrhagic shock (n = 2), myocardial infarction (n = 2), acute stroke (n = 1), or persistent sepsis (n = 1). Perioperative mortality was significantly higher in patients with endograft infection (6/12, p = 0.002) and in cases of supraceliac cross-clamping (4/6, p = 0.003). The association of infection with supraceliac cross-clamping was a strong predictor for perioperative mortality (p < 0.001).
CONCLUSION:
In our experience, endograft infection led to greater perioperative mortality after LOC. Recurrent aortoenteric fistula in association with supraceliac cross-clamping is a strong predictor of poor outcome. Patients surviving the perioperative period may have good chances of long-term survival
Mandibular subluxation as an adjunct in very distal carotid arterial reconstruction: incidence of peripheral and cerebral neurologic sequelae in a single-center experience.
No full textBackground: The location of the carotid bifurcation and a very distal extension of internal carotid atherosclerotic disease may challenge vascular surgeons performing carotid endarterectomy (CEA) by increasing technical difficulty and possibly the incidence of cranial nerve damage or palsies. The objective of the present study is to report on the safety of CEA with mandibular subluxation (MS) and to compare results of CEA in 2 groups of patients treated by standard CEA or by MS-CEA according to rates of major neurologic complications, death, and the occurrence of postoperative peripheral nerve palsy. Methods: Between July 2000 and June 2012, 1,357 CEAs were performed. MS was additionally used in 43 patients. Only patients with primary atherosclerotic internal carotid artery (ICA) lesions in the 2 groups (38 in the MS-CEA group and 1,289 in the standard CEA group) were considered for comparative analysis. Results: MS-CEA patients were more frequently male (P = 0.03), presented more frequently with symptomatic lesions (P = 0.007), longer lesions (P = 0.01), and had common ICA bypass implantation (P = 0.02). Mean follow-up was 68.75 +/- 37.87 months (range: 1-144 months). No perioperative neurologic mortality and no prolonged discomfort related to MS was recorded. The overall neurologic morbidity rate (major stroke/minor stroke/transient ischemic attach) was comparable in the 2 groups (P = 0.78). The overall immediate peripheral nerve injury rate was 7.89% in the MS-CEA group and 5.27% in the standard CEA group (P = 0.73). Three cases of permanent dysphonia in the standard CEA group (0.23%) and 1 case of dysphagia in the MS-CEA group (2.63%) were reported at follow-up (P = 0.24). Conclusions: MS-CEA can be a very useful technical adjunct for high-located carotid bifurcations or challenging carotid lesions, with an overall risk comparable to that of standard CEA
- …
