Tracheal Stenosis after Tracheostomy

INTRODUCTIONTracheal stenosis is a late and usually non-life threatening complication of surgical and percutaneous tracheostomies (PDT) as well as delayed endotracheal extubation.METHODSWe undertook a retrospective review of all patients who underwent a surgical tracheostomy over a 10 year period. Patients were included in the study if they had CT or MRI imaging of the tracheostomy site both pre-operatively and six or more weeks post operatively. Patients whose imaging was not available were excluded (n = 3) as were those patients who still had a tracheostomy in situ (n = 8). In total 91 patients were included in the study. In the same period 1170 surgical tracheostomies were performed by the maxillofacial surgeons. The images were analysed by a radiologist and the degree of stenosis reported.RESULTSAll 91 patients underwent a tracheostomy with a window. 83 patients did not demonstrate any stenosis. Looking at the remaining 8 patients with stenosis: 6 patients had stenosis of less than 25%, 1 patient had stenosis between 25-50% and 1 patient had stenosis greater than 50%. Both patients with stenosis greater than 25% had more than one surgical tracheostomy.CONCULSIONWe have shown that the risk of stenosis is 8.8%, lower than often quoted in literature, and when it occurs it is likely to be symptomatic only in severe stenosis. Our main risk of stenosis was repeat surgical tracheostomies which also seems to be linked to a greater degree of stenosis.     

Droplet fluid infusion into a dust layer in relation to self-cleaning

Wettability of a droplet liquid on a dusty hydrophobic plate is considered and the fluid infusion into the dust layer is studied pertinent to dust removal from the hydrophobic surfaces via rolling/sliding droplets. Influence of droplet hydrostatic pressure on the fluid infusion into dust layer is also investigated towards exploring the dust removal mechanisms. Environmental dust characteristics are evaluated and their interface with the droplet fluid is assessed. Sets of experiments are carried out to examine: (i) droplet fluid infusion into the dust layer, (ii) droplet fluid cloaking of dust, and (iii) evaluate the weight gain of the dust particles during cloaking. The findings reveal that droplet fluid (water) spreads onto the dusty surface and infuses on the dust particles. Cloaking velocity decays sharply with time and the weight gain of the dust particles is about 17% of the original dust weight after cloaking. The dust particles have a large area of nano-size open-pores-sites on the surface; however, capillary diffusion through these sites is limited with shallow depths and the weight gain of a dust particle via capillary diffusion is about 1% of the particle weight. The maximum infusion depth of the droplet fluid in the dust layer is about 74 μm, which is slightly less than the dust layer thickness on the surface. The rolling droplet picks up all the dust from the 150 μm thick dust layer on the surface.

Wettability of a droplet liquid on a dusty hydrophobic plate is considered and the fluid infusion into the dust layer is studied pertinent to dust removal from the hydrophobic surfaces via rolling/sliding droplets.     

MR Imaging–Detected Carotid Plaque Hemorrhage Is Stable for 2 Years and a Marker for Stenosis Progression

BACKGROUND AND PURPOSE:MR imaging–detected carotid plaque hemorrhage is associated with an increased risk of recurrent ischemic cerebrovascular events and could be an indicator of disease progression; however, there are limited data regarding the dynamics of the MR imaging–detected carotid plaque hemorrhage signal. We assessed the temporal change of this signal and its impact on carotid disease progression.MATERIALS AND METHODS:Thirty-seven symptomatic patients with 54 carotid stenoses of >30% on sonography underwent serial MR imaging during 24 months. A signal-intensity ratio of >1.5 between the carotid plaque and adjacent muscle was defined as plaque hemorrhage, and a change in signal-intensity ratio of >0.31 between time points was considered significant. Sixteen patients underwent ≥2 carotid sonography scans to determine the peak systolic velocities and degree of stenosis with time.RESULTS:Of the 54 carotids, 28 had the presence of hyperintense signal on an MR imaging sequence (PH+) and 26 had the absence of hyperintense signal on an MR imaging sequence (PH−) at baseline. The signal-intensity ratio was stable in 33/54 carotid plaques, but 39% showed a change. Plaque hemorrhage classification did not change in 87% of carotid plaques, but 4 became PH+, and 3, PH−. As a group, PH+ carotids did not change significantly in signal-intensity ratio (P = .585), whereas PH− showed an increased signal-intensity ratio at 24.5 months (P = .02). In PH+ plaques, peak systolic velocities significantly increased by 22 ± 39.8 cm/s from baseline to last follow-up sonography (Z = 2.427, P = .013).CONCLUSIONS:During 2 years, MR imaging–detected carotid plaque hemorrhage status remained stable in most (87%) cases with 4 (7%) incident plaque hemorrhages. PH+ plaques were associated with increased flow velocity during the follow-up period.

Currently, the degree of ICA stenosis is the principal criterion on the basis of which the decision for carotid intervention is made. This is based on strong evidence from randomized controlled trials that carotid endarterectomy reduces stroke risk in patients with severe carotid artery stenosis.^1,2 However, those studies also showed that a significant proportion of patients with symptomatic carotid disease will not have a recurrence. Subsequently, much research is focused on the identification of high-risk subgroups,³ especially for those with moderate or asymptomatic carotid stenosis.Plaque hemorrhage (PH) is implicated in carotid plaque vulnerability⁴ and is detectable by MR imaging.^5,6 A recent longitudinal follow-up study and meta-analysis⁷ demonstrated that MR imaging–detected plaque hemorrhage (MR imaging-PH) strongly predicts recurrent ischemic events. The MR imaging-PH signal seems to be stable for 12 months,⁸ but stability of MR imaging-PH features beyond 12 months remains unclear. Knowledge of longer term stability of MR imaging-PH would be helpful if it is to be used to assist decision-making in interventions and to determine the need for follow-up imaging.Plaque volume progression on sonography recently has been shown to predict cerebrovascular events⁹; however, this measure was not used in the current study. Carotid stenosis progression has been suggested to be a better predictor of subsequent TIA/stroke than a single measurement.¹⁰ Although general carotid sonography surveillance may not be cost-effective,¹¹ this situation may well be different for a subgroup of patients with a higher risk for stenosis progression. It is conceivable that MR imaging-PH is also an indicator of disease progression¹² and, therefore, may be useful in this regard.The aim of this study was to determine MR imaging signal changes in the carotid artery plaque during 2 years and whether the presence of MR imaging-PH at baseline is associated with stenosis progression.     

Intraplaque Hemorrhage and the Plaque Surface in Carotid Atherosclerosis: The Plaque At RISK Study (PARISK)

BACKGROUND AND PURPOSE:An important characteristic of vulnerable plaque, intraplaque hemorrhage, may predict plaque rupture. Plaque rupture can be visible on noninvasive imaging as a disruption of the plaque surface. We investigated the association between intraplaque hemorrhage and disruption of the plaque surface.MATERIALS AND METHODS:We selected the first 100 patients of the Plaque At RISK study, an ongoing prospective noninvasive plaque imaging study in patients with mild-to-moderate atherosclerotic lesions in the carotid artery. In carotid artery plaques, disruption of the plaque surface (defined as ulcerated plaques and/or fissured fibrous cap) and intraplaque hemorrhage were assessed by using MDCTA and 3T MR imaging, respectively. We used a χ² test and multivariable logistic regression to assess the association between intraplaque hemorrhage and disrupted plaque surface.RESULTS:One hundred forty-nine carotid arteries in 78 patients could be used for the current analyses. Intraplaque hemorrhage and plaque ulcerations were more prevalent in symptomatic compared with contralateral vessels (hemorrhage, 38% versus 11%; P < .001; and ulcerations, 27% versus 7%; P = .001). Fissured fibrous cap was more prevalent in symptomatic compared with contralateral vessels (13% versus 4%; P = .06). After adjustment for age, sex, diabetes mellitus, and degree of stenosis, intraplaque hemorrhage was associated with disrupted plaque surface (OR, 3.13; 95% CI, 1.25–7.84) in all vessels.CONCLUSIONS:Intraplaque hemorrhage is associated with disruption of the plaque surface in patients with a carotid artery stenosis of <70%. Serial studies are needed to investigate whether intraplaque hemorrhage indeed increases the risk of plaque rupture and subsequent ischemic stroke during follow-up.

The need to identify patients with mild-to-moderate carotid artery stenosis and an increased stroke risk who might benefit from surgical treatment has shifted research interest from assessment of the degree of carotid stenosis to assessment of vulnerable plaque characteristics.¹ Vulnerable plaques are atherosclerotic plaques more prone to rupture and are associated with a higher risk for thromboembolism and ischemic stroke.^2,3 Intraplaque hemorrhage is an important characteristic of the vulnerable plaque.⁴ Prevalence of intraplaque hemorrhage has been shown to be higher in symptomatic than in asymptomatic lesions.⁵ Moreover, the presence of intraplaque hemorrhage in carotid artery disease is associated with an increased risk of cerebral ischemic events.^6–8The pathophysiologic mechanism leading to intraplaque hemorrhage is a topic of debate. However, a common viewpoint is that small leaky neovessels in the atherosclerotic plaques are a likely source of intraplaque hemorrhage.^5,9,10 The presence of intraplaque hemorrhage is thought to initiate several biologic processes like phagocytosis and local inflammation, leading to the release of proteolytic enzymes, deposition of free cholesterol and subsequently plaque growth, plaque destabilization, and possible plaque rupture.^5,9–12 Plaque rupture can be visible on imaging as a disruption of the atherosclerotic plaque surface (plaque ulceration and/or a fissured fibrous cap).^13,14 A previous study reported that plaque ulceration on CTA was useful for the prediction of intraplaque hemorrhage on MR imaging in a broad group of symptomatic patients referred for carotid artery imaging.¹⁵ Ulcerated plaques themselves are independently associated with an increased risk of ipsilateral ischemic events as well.^16,17The aim of the current study was to investigate the association between intraplaque hemorrhage, as assessed on MR imaging, and disruption of the plaque surface, assessed on MDCTA, in symptomatic patients with a carotid artery stenosis of <70%.