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0.25–11% of patients who sustain a single long-bone fracture meet the criteria of FE 5, 8, 9. An autopsy study of soldiers who died in the Second World War revealed a 65% incidence of pulmonary fat droplets 7. Embolisation of bone fat probably occurs in almost all patients who sustain a pelvic or long-bone fracture or undergo an endomedullary nailing of long-bone fractures or placement of knee and hip prosthesis 6.
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This article reviews the features of acute and chronic NTPE.ĭisruption of sinusoids and fat in bone marrow allows fat globules and bone debris to gain access to the venous circulation. Nevertheless, NTPE can be associated with specific imaging findings, and familiarity with these features should facilitate prompt diagnosis 3. This implies that the pathogenesis of NTPE is more complex than that of pulmonary thromboembolism and it is subject to continued speculation 2. In contrast to “ordinary” thrombotic pulmonary embolism (PE), the effects of NTPE are not purely mechanical but are also linked to the nature of the embolic agent. Different cell types (adipocyte, haematopoietic, amniotic, trophoblastic or tumour), bacteria, fungi, foreign material and gas may be carried in the bloodstream and embolise to the pulmonary circulation (fig. 1 ⇓). NTPE often presents with uncharacteristic clinical features and requires peculiar diagnostic measures and treatment options. Unlike pulmonary thromboembolism, a frequently encountered cause of morbidity and mortality 1, nonthrombotic pulmonary embolism (NTPE) is less common. Despite the fact that detailed descriptions of several forms of NTPE have existed for nearly 100 years, well-designed trials have never been performed to evaluate therapy in the different subsets of these patients.
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Increased awareness of NTPE as an underestimated cause of acute and chronic embolism, which may result in acute and chronic pulmonary hypertension, is needed. Thin-section computed tomography of the lungs showing peculiar radiographic findings, such as a feeding vessel, the so-called tree-in-bud pattern or the appearance of micronodules distributed at the termination of bronchovascular bundles, may be observed in certain forms of NTPE. Here, we also aim to familiarise the reader with the atypical radiological features of NTPE. Frequently, lung biopsies revealing severe granulomatous reaction or unfortunate post-mortem pathological investigations of pulmonary tissue are necessary to confirm the diagnosis. Pathological observations play a key role in the exact diagnosis, and sometimes carefully aspirated blood from the pulmonary artery or specific staining of cells recovered from bronchoalveolar lavage fluid may be helpful. They range from very dramatic acute presentations such as acute respiratory distress syndrome to signs observed late in the disease course. NTPE presents a formidable diagnostic challenge, as the condition often presents with very unusual and peculiar clinical signs that are frequently overlooked. Nonthrombotic emboli may also lead to a severe inflammatory reaction both in the systemic and pulmonary circulation, as well as in the lung. The complex and diverse pathogenesis of different subtypes of emboli is subject to continuing speculation and is certainly far more complex than “simple” mechanical obstruction after embolisation of vascular thrombi. The purpose of this article is to describe the clinical signs, pathogenesis, diagnosis and treatment of the different NTPE subtypes.
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Nonthrombotic pulmonary embolism (NTPE) is defined as embolisation to the pulmonary circulation of different cell types (adipocytes, haematopoietic, amniotic, trophoblastic or tumour), bacteria, fungi, foreign material or gas.