Intravascular embolization of device fragments is a rare but potentially serious complication.
A systematic search of the PubMed and MEDLINE databases for all articles pertaining to central catheter ...related embolization published in English between 1985 and 2007 was made.
A total of 215 cases of intravenous catheter embolization were identified. There were 143 totally implanted venous devices (TIVD) or port catheters and 72 percutaneous venous catheters (PVC). Sites of catheter fragments following embolization were the superior vena cava or peripheral veins (15.4%), the right atrium (27.6%), right ventricle (22%), and pulmonary arteries (35%). Clinical signs of catheter embolization included catheter malfunction (56.3%), arrhythmia (13%), pulmonary symptoms (4.7%), and septic syndromes (1.8%), but 24.2% of cases were asymptomatic. The causes of intravascular catheter embolization were pinch-off syndrome (40.9%), catheter injury during explantation (17.7%), catheter disconnection (10.7%), and catheter rupture (11.6%). In 19.1% of cases, the cause of catheter embolization could not be identified. Most embolized catheter fragments (93.5%) were removed percutaneously. In 4.2% of cases, fragments were retained in the vascular bed; in 2.3%, embolized fragments were removed surgically via thoracotomy.
Intravascular catheter embolization can go undiagnosed for prolonged periods. Patients might be asymptomatic or may develop severe systemic clinical signs. The mortality rate is 1.8%. There were no significant differences in clinical features of embolization between TIVD and PVC groups.
Abstract Background Several studies in patients with acute myocardial infarction (AMI) without cardiogenic shock (CS) indicate a better survival in smokers, the so called “smoker’s paradox”. For CS, ...this relationship has not been investigated so far in the primary percutaneous coronary intervention (PCI) era. Methods In a predefined substudy of the Intraaortic Balloon Pump in Cardiogenic Shock II (IABP-SHOCK II) trial and its accompanying registry including patients with CS complicating AMI we investigated differences in outcome of smokers compared to non-smokers. All-cause-mortality at 1 year was used as primary endpoint. Results Of 772 patients with available smoking status 263 patients were smokers (34%). Smokers were more often male (79% vs. 65%; p < 0.001), of younger age (61 interquartile range IQR 52-70 vs. 73 IQR 64-79 years; p < 0.001), had less comorbidity including arterial hypertension (62% vs. 71%; p = 0.007) and diabetes mellitus (26% vs. 38%; p < 0.001) and had lower levels of serum creatinine (13% vs. 25%; p < 0.001). There was no significant difference between the 2 groups regarding left ventricular ejection fraction, initial revascularization strategy or use of IABP. Smokers had lower rates of mortality at 12 months in univariable analysis (43% vs. 59%; p < 0.001) but not after adjustment for important confounders using Cox-regression analysis (hazard ratio 0.77, 95% confidence interval 0.59-1.03; p = 0.08). Conclusion Smoking is not predictive of outcome in patients with CS complicating AMI. The observed survival benefit in univariable analysis seems to be explained by the younger age and lower risk profile of smokers.
Acute kidney injury (AKI) is associated with an increased mortality in critically ill patients, especially in patients with multiorgan dysfunction syndrome (MODS). In daily clinical practice, the ...grading of AKI follows the Kidney Disease: Improving Global Outcomes (KDIGO) criteria. In most cases, a relevant delay occurs frequently between the onset of AKI and detectable changes in creatinine levels as well as clinical symptoms. The aim of the present study was to examine whether a near infrared spectroscopy (NIRS)-based, non-invasive ischemia-reperfusion test (vascular occlusion test (VOT)) together with unprovoked (under resting conditions) tissue oxygen saturation (StO
) measurements, contain prognostic information in the early stage of MODS regarding the developing need for renal replacement therapy (RRT).
Within a period of 18 months, patients at the medical intensive care unit of a tertiary university hospital with newly developed MODS (≤24 h after diagnosis, APACHE II score ≥20) were included in our study. The VOT occlusion slope (OS) and recovery slope (RS) were recorded in addition to unprovoked StO
. StO
was determined non-invasively in the area of the thenar muscles using a bedside NIRS device. The VOT was carried out by inflating a blood pressure cuff on the upper arm. AKI stages were determined by the changes in creatinine levels, urinary output, and/or the need for RRT according to KDIGO.
56 patients with MODS were included in the study (aged 62.5 ± 14.4 years, 40 men and 16 women, APACHE II score 34.5 ± 6.4). Incidences of the different AKI stages were: no AKI, 16.1% (
= 9); AKI stage I, 19.6% (
= 11); AKI stage II, 25% (
= 14); AKI stage III, 39.3% (
= 22). Thus, 39.3% of the patients (
= 22) developed the need for renal replacement therapy (AKI stage III). These patients had a significantly higher mortality over 28 days (RRT, 72% (
= 16/22) vs. no RRT, 44% (
= 15/34);
= 0.03). The mean unprovoked StO
of all patients at baseline was 81.7 ± 11.1%, and did not differ between patients with or without the need for RRT. Patients with RRT showed significantly weaker negative values of the OS (-9.1 ± 3.7 vs. -11.7 ± 4.1%/min,
= 0.01) and lower values for the RS (1.7 ± 0.9 vs. 2.3 ± 1.6%/s,
= 0.02) compared to non-dialysis patients. Consistent with these results, weaker negative values of the OS were found in higher AKI stages (no AKI, -12.7 ± 4.1%/min; AKI stage I, -11.5 ± 3.0%/min; AKI stage II, -11.1 ± 3.3%/min; AKI stage III, -9.1 ± 3.7%/min;
= 0.021). Unprovoked StO
did not contain prognostic information regarding the AKI stages.
The weaker negative values of the VOT parameter OS are associated with an increased risk of developing AKI and RRT, and increased mortality in the early phase of MODS, while unprovoked StO
does not contain prognostic information in that regard.
Background
According to the “Third Universal Definition of Myocardial Infarction”, cardiac troponin (cTn) is defined to be elevated, if the value is above the 99th percentile of a normal reference ...population. Especially in emergency medicine, this leads to pathological values more often than before this definition has been founded. Severe sepsis and septic shock frequently cause a rise of cTn, but there is only limited data about its role in septic patients in the emergency department (ED). Therefore, we investigated the frequency, main causes, and prognostic relevance of elevated high-sensitive troponin T (hsTnT) in septic patients in the ED.
Methods
Adults presenting at the ED with sepsis were included in the study. HsTnT was measured soon after admission. Main influencing factors were investigated, and the prognostic value was evaluated.
Results
197 of the 313 analysed patients (62.9 %) showed an elevated hsTnT, with significantly higher rates in patients with severe sepsis and septic shock than in uncomplicated sepsis. APACHE II score, creatinine, and coronary heart disease were found to influence hsTnT independently. Nevertheless, patients with uncomplicated sepsis and without relevant renal insufficiency also showed notable rates of elevated hsTnT: 51.6 % (uncomplicated sepsis) and 34.5 % (no relevant renal failure), respectively. HsTnT showed a prognostic value with higher levels in non-survivors and an AUC of 0.72,
p
< 0.001.
Conclusions
In the ED, sepsis is a relevant cause of elevated cTn, which underlines the role of sepsis as a differential diagnosis in non-ACS patients with positive cTn. A rise of cTn may be an indicator of poor outcome.
Background: A reduced heart rate variability (HRV) is associated with worse prognosis, increased incidence of cardiovascular disease (CVD) and mortality. There are conflicting results and a lack of ...population-based data regarding the association of HRV with CVD risk factors and its potential role as independent cause or mediator of CVD risk. Methods: Cross-sectional data of a population-based cohort including 1,779 women and men aged 45-83 years were used to analyse associations of time and frequency domain measures of HRV (derived from 5-min ECG segments) with age, behavioural and biomedical risk factors and disease in the whole sample and in a “healthy” subgroup. Results: Age was inversely associated with all measures of HRV (mean standard deviation of normal intervals across 10-year age-groups 32.1, 26.9, 27.1 and 24.8 ms in women, 29.3, 25.9, 23.8 and 25.7 ms in men). There was no association of physical activity, current smoking or alcohol with HRV. In age-adjusted models, triglycerides, glucose, waist-to-hip ratio and diabetes were inversely associated with HRV in men and women, and low/high density cholesterol and hypertension in men only (up to 43% difference across risk factor quartiles). Multivariable adjustment and restriction to the “healthy” subgroup attenuated the associations. Conclusions: We found only weak and inconsistent associations of HRV with cardiovascular risk factors. However, these results as well as those from previous studies are still compatible with the hypothesis that short-term HRV may be a marker of ill health or a mediator of the effect of selected biomedical risk factors on CVD.
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Introduction
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Atherosclerosis ‐ overview
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General remarks
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Early atherosclerosis
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Exogenous and/or infectious activators
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Endogenous activators
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Later phases of atherosclerosis
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...Innate and inflammatory pathways in atherogenesis
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Innate receptors
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PAMP and DAMP
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Pentraxins
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NOD‐like proteins/receptors (NLRs)
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toll‐like receptors (TLRs)
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Knockout of pattern recognition molecules reduces atherosclerosis
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Innate cytokines
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The innate cytokines interleukin‐1 (IL‐1) and tumor necrosis factor‐α (TNF‐α)
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TNF−/− ApoE−/− mice are less atherosclerotic
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IL‐1−/− ApoE−/− mice are less atherosclerotic
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Monocyte chemoattractant protein‐1 and fractalkine
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IL‐6 activates innate pathways and is produced by cardiovascular cells
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Functions of IL‐6 important for atherogenesis
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Role of trans‐signalling in cardiovascular inflammation
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Animal experiments suggest a role for the IL‐6 system in atherosclerosis
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Cytokine‐mediated interaction of vessel wall cells and leucocytes
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Endothelial cell (EC)‐monocyte interaction
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Smooth muscle cell (SMC)‐EC interaction
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SMC‐monocyte and SMC‐T cell interaction
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Summary and conclusion
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Future perspectives
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Which initiator(s) starts atherogenesis?
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Is there more than one starting point?
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What are the specific roles of the various cytokines in the vessel wall?
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Are treatments addressing different phases of atherogenesis of advantage?
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What about prevention?
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What are the expectations?
Inflammation is a central element of atherogenesis. Innate pathways contribute to vascular inflammation. However, the initial molecular process(es) starting atherogenesis remain elusive. The various risk factors, represented by particular compounds (activators), may cause altered cellular functions in the endothelium (e.g. vascular endothelial cell activation or ‐dysfunction), in invading cells (e.g. inflammatory mediator production) or in local vessel wall cells (e.g. inflammatory mediators, migration), thereby triggering the innate inflammatory process. The cellular components of innate immunology include granulocytes, natural killer cells and monocytes. Among the molecular innate constituents are innate molecules, such as the toll‐like receptors or innate cytokines. Interleukin‐1 (IL‐1) and IL‐6 are among the innate cytokines. Cytokines are potent activators of a great number of cellular functions relevant to maintain or commove homeostasis of the vessel wall. Within the vessel wall, vascular smooth muscle cells (SMCs) can significantly contribute to the cytokine‐dependent inflammatory network by: (i) production of cytokines, (ii) response to cytokines and (iii) cytokine‐mediated interaction with invading leucocytes. The cytokines IL‐1 and IL‐6 are involved in SMC‐leucocyte interaction. The IL‐6 effects are proposed to be mediated by trans‐signalling. Dysregulated cellular functions resulting from dysregulated cytokine production may be the cause of cell accumulation, subsequent low‐density lipoprotein accumulation and deposition of extracellular matrix (ECM). The deposition of ECM, increased accumulation of leucocytes and altered levels of inflammatory mediators may constitute an ‘innate‐immunovascular‐memory’ resulting in an ever‐growing response to anew invasion. Thus, SMC‐fostered inflammation, promoted by invading innate cells, may be a potent component for development and acceleration of atherosclerosis.
To examine end-of-life (EOL) practices in European ICUs: who makes these decisions, how they are made, communication of these decisions and questions on communication between the physicians, nurses, ...patients and families.
Data collected prospectively on EOL decisions facilitated by a questionnaire including EOL decision categories, geographical regions, mental competency, information about patient wishes, and discussions with patients, families and health care professionals.
37 European ICUs in 17 countries.
ICU physicians collected data on 4,248 patients.
95% of patients lacked decision making capacity at the time of EOL decision and patient's wishes were known in only 20% of cases. EOL decisions were discussed with the family in 68% of cases. Physicians reported having more information about patients' wishes and discussions in the northern countries (31%, 88%) than central (16%, 70%) or southern (13%, 48%) countries. The family was more often told (88%) than asked (38%) about EOL decisions. Physicians' reasons for not discussing EOL care with the family included the fact that the patient was unresponsive to therapy (39%), the family was unavailable (28%), and the family was thought not to understand (25%).
ICU patients typically lack decision-making capacity, and physicians know patients' wishes in only 20% of EOL decisions. There were regional differences in discussions of EOL decisions with families and other physicians. In European ICUs there seems to be a need to improve communication.
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