In the practice of forensic pathology, fat embolism is one of the common causes of death, which can be divided into two categories: traumatic and non-traumatic. Non-traumatic fat embolism refers to the blockage of small blood vessels by fat droplets in the circulatory blood flow caused by non-traumatic factors such as underlying diseases, stress, poisoning and lipid metabolism disorders. At present, it is believed that the production of non-traumatic fat embolism is related to the disturbance of lipid metabolism, C-reactive protein-related cascade reaction, the agglutination of chylomicron and very low-density lipoprotein. The forensic identification of the cause of death of non-traumatic fat embolism is mainly based on the case, systematic autopsy, HE staining and fat staining, but it is often missed or misdiagnosed by forensic examiners because of its unknown risk factors, hidden onset, the difficulty of HE staining observation and irregular implementation of fat staining. In view of the lack of attention to non-traumatic fat embolism in forensic identification, this paper reviews the concepts, pathophysiological mechanism, research progress, existing problems and countermeasures of non-traumatic fat embolism, providing reference for forensic scholars.
Autopsy ; Embolism, Fat/pathology* ; Forensic Medicine ; Forensic Pathology ; Humans ; Pulmonary Embolism/pathology*

This study was done to demonstrate the computed tomography (CT) and pathologic findings of the sequential changes for experimental pulmonary fat embolism (PFE), and to correlate the CT and pathologic findings of rabbit lung. PFE was induced by an intravenous injection of 0.2 mL linoleic acid in 24 rabbits. The rabbits were divided into 4 groups of 6 rabbits each. CT scans were obtained sequentially at 2 hr (n= 24), day 1 (n=18), day 3 (n=12) and day 7 (n=6) after fat embolization. The pathologic findings were analyzed and CT-pathologic correlation was done. CT scans showed bilateral ground-glass opacity (GGO), consolidation and nodule in all cases. The findings of PFE at 2 hr after fat embolization were areas of decreased attenuation, GGO, consolidation and nodule. These findings were aggravated on the follow- up CT after 1 day and 3 days. The follow-up CT revealed linear density in the subpleural lungs after 7 days. On CT-pathology correlation, wedge-shaped ischemic necrosis in the subpleural lungs correlated with nodule at 2 hr. GGO and consolidation at day 1 on CT correlated with congestion and edema, and these findings at day 3 were correlated with inflammation and hemorrhagic edema. The linear density in the subpleural lungs correlated with interstitial fibrosis and pleural contraction at day 7. In conclusion, PFE was caused by using linoleic acid which is kind of free fatty acid and this study served as one model of the occurrence of nontraumatic PFE. CT accurately depicted the natural evolution of PFE in the serial followup, and this correlated well with the pathologic findings.
Animals ; Embolism, Fat/*pathology/*radiography ; Pulmonary Embolism/*pathology/*radiography ; Rabbits ; *Tomography, X-Ray Computed

Air embolism, a life-threatening complication of medical procedure, is a frequently encountered challenge in the forensic practices. It can be easily missed due to ignorance by forensic examiner or it could be difficult to be identified due to prolonged storage of the cadaver. This article reviews the etiological factors, pathophysiological changes, clinical manifestation, diagnosis, and the medicolegal identification of air embolism. The authors suggest that modern imaging techniques including echocardiogram, computer tomography, and magnetic resonance imaging play animportant role in the clinical diagnosis and forensic identification of air embolism.
Cause of Death ; Echocardiography ; Embolism, Air/pathology* ; Forensic Pathology ; Humans ; Postmortem Changes ; Pulmonary Embolism/etiology* ; Tomography, X-Ray Computed

Cytokines ; immunology ; Embolism ; immunology ; metabolism ; pathology ; Endometriosis ; immunology ; metabolism ; pathology ; Female ; Hormones ; metabolism ; Humans

It is widely accepted that endoscopic submucosal dissection (ESD) is an important treatment option for cases of early gastric carcinoma where the probability of lymph node metastasis is very low. The resected ESD specimens are carefully examined by serial sections at 2 mm intervals, and if pathology reveals submucosal invasion more than 500microm and/or lymphovascular invasion, or if the resection margin is involved by the tumor, surgery is recommended. In this point of view, thorough pathologic examination and reporting the accurate pathologic diagnosis of ESD specimen is very important. The diagnostic approach and pitfalls in the diagnosis of ESD specimen are reviewed.
*Dissection ; Embolism/pathology ; Endoscopy, Gastrointestinal ; Gastric Mucosa/*pathology/surgery ; Humans ; Lymphatic Metastasis/pathology ; Stomach Neoplasms/*pathology/surgery

BACKGROUNDThe experimental studies of venous thromboembolism (VTE) as an entity and the response of the pulmonary arterial endothelium after VTE are still rare. The objective of this study was to observe changes in the pulmonary arterial endothelium using a novel rat model of VTE.

METHODSRats were allocated to the VTE (n = 54) or control groups (n = 9). The left femoral vein was blocked using a microvessel clip to form deep vein thrombosis (DVT). One, four or seven-day-old thrombi were injected into the right femoral vein to induce DVT-pulmonary thromboembolism (DVT-PTE). The rats were sacrificed 1, 4 or 7 days later (D(n(1,4,7)) P(n(1,4,7)) subgroups (n = 6)), and the lungs were examined using light and electron microscopy.

RESULTSOn gross dissection, the rate of DVT formation was higher on day 1 (D(1)P(n): 100%, 18/18) than day 4 (D(4)P(n): 83%, 15/18; χ(2) = 5.900, P = 0.015) or day 7 (D(7)P(n): 44%, 8/18; χ(2) = 13.846, P = 0.000). On gross dissection, the positive emboli residue rate in the pulmonary arteries was lower in the D(1)P(n) subgroup (39%, 7/18) than the D(4)P(n) (73%, 11/15; χ(2) = 3.915, P = 0.048) and D(7)P(n) subgroups (100%, 8/8; χ(2) = 8.474, P = 0.004); however, light microscopy indicated the residual emboli rate was similar in all subgroups. Hyperplasia of the pulmonary arterial endothelium was observed 4 and 7 days after the injection of one-day-old or four-day-old thrombi. However, regions without pulmonary arterial endothelial cells and intra-elastic layers were observed one day after injection of seven-day-old thrombi.

CONCLUSIONSThis novel model closely simulates the clinical situations of thrombus formation and is ideal to study pulmonary endothelial cell activation. The outcome of emboli and pulmonary arterial endothelial alterations are related to the age and nature of the thrombi.

Animals ; Disease Models, Animal ; Endothelium, Vascular ; pathology ; Pulmonary Artery ; pathology ; Pulmonary Embolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Venous Thromboembolism ; pathology

OBJECTIVETo study thrombosis and its significance after acute experimental pulmonary thromboembolism.

METHODSThe acute pulmonary thromboembolism (PTE) model of rabbits was established by intravenous injection of autologous blood clots (0.04 g/kg) which were stabilized in temperature-controlled (70 degrees C) distilled water for 10 min. The process of thrombosis was observed grossly and microscopically. The Quick's method was used to examine the coagulability of blood and radioimmunoassay was employed to measure the level of plasma thromboxane A(2) and endothelin.

RESULTSThrombotic propensity was observed at 1 h, fresh thrombus started to form and the blood coagulation system was activated at 24 h following clots infusion. Emboli were completely or partly dissolved at 5 d and appeared to organize at both 10 d and 14 d after clots were infused. Venous plasma thromboxane A(2) concentration began to increase at 5 min (2489.59 +/- 714.68 ng/L) and reached its maximum at 15 min (2545.46 +/- 590.58 ng/L) then declined at 60 min after clot infusion (P < 0.001, respectively, vs 626.59 +/- 510.02 ng/L of pre-clot). The level of endothelin in both arterial and venous blood increased at 5 d post-clot infusion (840.74 +/- 154.19 ng/L, 230.35 +/- 52.39 ng/L, respectively) compared to the one before infusion (602.66 +/- 453.26 ng/L, 148.01 +/- 53.28 ng/L, respectively, P < 0.05).

CONCLUSIONSThrombosis occurs after autologous-blood-clot-induced PTE. The interactions between thrombus formation, fibrinolysis and organization determines the consequences of emboli. Abnormalities of endothelin metabolism and the increment of thromboxane A(2) may play an important role in PTE.

Animals ; Blood Coagulation ; Endothelins ; blood ; Lung ; pathology ; Pulmonary Embolism ; blood ; pathology ; Rabbits ; Thrombosis ; pathology ; Thromboxane B2 ; blood

OBJECTIVE: To explore the related risk facts of pulmonary thromboembolism (PTE) and analyze the relation between PTE and the trauma or medical behavior by investigating the cases of PTE. METHODS: Thirty-three cases were selected from Institute of Forensic Science (IFS) from 2000 to 2014. RESULTS: In 33 cases, 16 decedents were male, 17 decedents were female; different degrees of dyspnea, chest tight- ness and syncope symptoms were the clinical manifestation of the deceased; the thrombus was mainly distributed in the left and right pulmonary arteries. The main source of embolism was the deep vein of lower limb and the left probability was higher. Trauma, limited position, operation and cardiovascular disease showed high-risk factors of PTE; D-Dimer test, hemolytic test and computer tomography pul- monary angiography were the diagnostic tools for PTE. In some cases, trauma and medical malpractice could be involved in the cause of death. CONCLUSION Non-typical clinical symptoms present in the most cases caused by PTE, and these cases always show many high-risk factors. The relation between PTE and injury or medical behavior should be considered carefully in the forensic pathological practice.
Female ; Fibrin Fibrinogen Degradation Products/chemistry* ; Forensic Pathology ; Humans ; Lower Extremity/pathology* ; Lung/pathology* ; Male ; Malpractice ; Pulmonary Embolism/mortality*

PURPOSE: To elucidate high-resolution CT(HRCT) findings and their pathologic basis in pulmonary oil embolism induced by LipiodoI-Adriamycin emulsion. MATERIALS AND METHODS: Pulmonary oil embolism was induced by infusing LipiodoI-Adriamycin emulsion through a peripheral vein in twelve Yorkshire pigs. Serial HRCT scans were performed on 2rid, 4th, 7th, 14th, and 28th day after the procedure. The pigs were sacrificed immediately after HRCT and histologic specimens were prepared in the same plane and level with HRCT. RESULTS: The basic pathology was reversible hemorrhagic edema of the lung. On HRCT, intraalveolar hemorrhage and edema in the acute stage manifested as ground-glass opacity or air-space consolidation of the whole secondary Iobule. The lesions were predominantly distributed over the dependent posterior lung fields because the specific gravity of Lipiodol is 1.28. Interlobular septal thickening due to edematous fluid collection was also associated. With the elapse of time, the extent and severity of the acute lesions resolved and, sometimes, changed into small nodular opacities. Pulmonary opacity was most severe on the post-embolization 2nd day and completely resolved within 2 weeks. CONCLUSION: Pulmonary embolization of LipiodoI-Adriamycin emulsion causes reversible hemorrhagic edema of the lung and Lipiodol toxicity seems to play a major role. HRCT findings of pulmonary oil embolism are quite different from those of pneumonia and pulmonary metastasis, which suggests the possibility of clincal application.
Edema ; Embolism* ; Ethiodized Oil ; Hemorrhage ; Lung ; Neoplasm Metastasis ; Pathology ; Pneumonia ; Specific Gravity ; Swine ; Veins

Aged, 80 and over ; Aorta, Abdominal ; pathology ; Embolism, Cholesterol ; therapy ; Female ; Humans