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Claus Kroegel

Publications and source records attributed to Claus Kroegel.

27 records · Page 2Linked to original sources

Transthoracic sonography of diffuse parenchymal lung disease: the role of comet tail artifacts.

OBJECTIVE: The value of transthoracic sonography in diffuse parenchymal lung disease is not established. This prospective study was conducted to analyze pleural and parenchymal alterations in patients with diffuse parenchymal lung disease by transthoracic sonography and to compare the results with the findings of a control group. METHODS: Fifty-three patients with diffuse parenchymal lung disease and 35 control subjects underwent transthoracic sonography for assessment of (1) basal pleural effusion, (2) the presence and number of comet tail artifacts, (3) thickening, (4) an irregular, fragmented pleural line, and (5) subpleural alterations. RESULTS: Basal pleural effusion was revealed in 37.7% of the patients with diffuse parenchymal lung disease (0% of the control subjects; P < .001), and 98.1% had multiple (>6 per scan) comet tail artifacts (14.3% of the control subjects; P < .001). Only a few artifacts (< or = 6 per scan; P < .001) were shown in 85.7% of the control subjects. All the control subjects had strongly localized comet tail artifacts and no thickened pleural line (84.9% of patients; P < .001). In 98.1 % of the patients, an irregular, fragmented pleural surface could be detected (82.8% of the control subjects; P < .05). Subpleural alterations were found in 37.7% of the patients and in 8.6% of the control subjects (P < .001). CONCLUSIONS: Diffuse parenchymal lung disease should be considered if multiple comet tail artifacts distributed over the whole surface of the lung together with a thickened and irregular, fragmented pleural line are visible. Transthoracic sonography may reflect the distribution of pleural involvement and may show subpleural alterations.

Artifacts↗

Principle mechanisms underlying venous thromboembolism: epidemiology, risk factors, pathophysiology and pathogenesis.

Deep vein thrombosis (DVT) and pulmonary embolism (PE) are distinct but related aspects of the same dynamic disease process known as venous thromboembolism (VTE). An estimated 200,000 new cases occur in the United States every year, including 94,000 with PE, resulting in an incidence of 23 per 100,000 patients per year-cases. Without treatment, pulmonary embolism is associated with a mortality rate of approximately 30%, causing nearly 50,000 deaths per year. Moreover, based on post-mortem studies, two-thirds of the patients with pulmonary emboli remain undiagnosed. Clinically, PE may present as (1) isolated dyspnea, (2) pleuritic pain and/or hemoptysis, and (3) circulatory collapse. However, clinical history and examination can be notoriously misleading in reaching a diagnosis. A number of acquired etiologic risk factors (predispositions) are associated with a tendency to develop VTE. These include increasing age, immobilization, surgery, trauma, hospital or nursing home confinement, malignancy, neurologic disease with extremity paresis, as well as certain types of oral contraception and hormone replacement therapy. In addition, a variety of genetic risk factors, such as factor V Leiden, protein S or C deficiency have also been identified. However, in at least half of the instances, no predisposing factors can be identified (idiopathic PE). In the majority of cases thromboemboli originate in the deep veins of the calf or pelvis. The pathogenic conditions for VTE comprise a triad of factors and include (1) venous stasis, (2) hypercoagulable states, and (3) vascular endothelium injury. Occlusion of pulmonary arteries has variable and transient clinical and pathophysiologic consequences, involving both mechanical and reflex effects of vascular occlusion with a consecutive perfusion defect as well as the release of vasoactive and other inflammatory mediators. The objectives of this article are to present an overview of the etiologic and pathogenic factors promoting VTE as well as the pathophysiologic and inflammatory processes following PE.

Comorbidity↗

Transthoracic ultrasound of lung and pleura in the diagnosis of pulmonary embolism: a novel non-invasive bedside approach.

The diagnosis of pulmonary embolism (PE) presents a considerable challenge and requires a high index of clinical suspicion from the attending physician. In addition, diagnosing PE may require the use of one or more direct and indirect diagnostic methods. Here, transthoracic sonography (TS) provides an alternative and attractive bedside approach which is based on (1) detecting alterations in the lung parenchyma, (2) involvement of the pleura and (3) peripheral perfusion characteristics associated with thromboembolism. Using a 5 MHz or 3.5 MHz convex scanner, occasionally supplemented by a 7.5 MHz linear scanner or colour-flow Doppler mode, the intercostal areas are systematically examined by TS. Most of the PE-related lesions are localised in the lower lobes of the lung and are often associated with an area of pleuritic chest pain. The characteristic sonographic findings of TS in PE are multiple, hypoechoic, pleural-based parenchymal lesions which adopt a wedge-shape. In addition, a central echo may occasionally be detectable within the lesion. Another regular sonographic feature is the involvement of the pleura manifesting as either localised effusion, basal effusion or both. However, several differential diagnoses such as pneumonia, bronchogenic carcinoma, metastases of extra-pulmonary malignancies, and simple pleurisy need to be excluded. Since localisation of PE-associated lesions may occasionally escape sonographic detection, an inconspicuous sonographic result does not fully exclude PE. As detection of PE-associated lesions using chest ultrasonography has a high specificity and sensitivity, can be rapidly performed, is widely available, non-invasive, cost-effective, and avoids transport of critically ill patients to the investigation site, the technique may prove a valuable tool in the diagnosis of PE at bedside facilitating immediate treatment decision. Further, because the method focuses on detection of peripheral lesions it complements other diagnostic techniques employed when PE is suspected.

Carcinoma, Bronchogenic↗