1/11. Massive fat and necrotic bone marrow embolization in a previously undiagnosed patient with sickle cell disease.A case of sickle cell disease diagnosed postmortem is described. A 37-year-old black woman presented with anemia, respiratory distress, and abdominal and back pain. death followed an intramuscular injection of iron, and anaphylaxis was clinically diagnosed. At autopsy, massive fat and necrotic bone marrow embolization of pulmonary and renal vessels was found. In the vertebral column, multifocal areas of ischemic necrosis were present, and proved to be the source of this embolization. Sickled red cells appeared in bone marrow sinusoids, and signs of disseminated intravascular coagulation were present.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/11. Marrow embolus to posterior ciliary vessel.A 69-year-old man with respiratory disease sustained multiple rib fractures during resuscitation for respiratory arrest. death occurred after the second attempt. autopsy findings included carcinoma of the lung with widespread metastases, multiple pulmonary marrow emboli, and a marrow embolus to the posterior ciliary vessel.- - - - - - - - - - ranking = 5keywords = vessel (Clic here for more details about this article) |
3/11. Fat embolism to the cardiac conduction system associated with sudden death.During a brief hospital stay, a patient under treatment with corticosteroids for lymphoma died suddenly and unexpectedly. At autopsy, fat emboli were identified in the lungs, myocardium, liver, and brain. Examination of the cardiac conduction system revealed fat emboli in the vessels of the bundle of his as well as those accompanying the bundle branches, a finding believed to have resulted in the sudden death. This report is the first of fat embolization to the cardiac conduction system and emphasizes the importance of examination of this system in cases of unexplained or sudden death.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
4/11. Acquired angiodysplasia as a cause of gastric hemorrhage: a possible consequence of cholesterol embolization.A patient with aortic stenosis and gastrointestinal bleeding due to angiodysplastic (telangiectatic) lesions in the stomach is presented. biopsy of the lesions showed cholesterol emboli with granuloma formation, intramucosal vascular obstruction, subepithelial ectatic vessels, and epithelial atrophy. The case history appeared to indicate the formation of new lesions over time and a tendency to a regression of some of the least advanced lesions. It is suggested that cholesterol showers from the aortic valve or atheromatous aortic plaques may be one cause of acquired angiodysplastic lesions in the gastrointestinal tract.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
5/11. Diffuse disseminated atheroembolism. Three cases with neuro-ophthalmic manifestation.Neuro-ophthalmic manifestations led to the diagnosis of diffuse disseminated atheroembolism (DDA) in three men whose systemic symptoms had remained unexplained for years. The cholesterol emboli that cause DDA originate from friable plaques in the aorta and great vessels. Ophthalmologists should be alert to the diagnosis of DDA in patients with elevated ESRs, stroke, transient amaurosis, or cholesterol emboli in the fundi. early diagnosis is important because arteriography, endarterectomy, and anticoagulation seem to increase the risk of serious, even fatal, embolization in these patients.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
6/11. The clinical spectrum of renal cholesterol embolization.Renal cholesterol embolization can occur spontaneously or as a complication of aortic surgery or major vessel angiography in patients with diffuse atherosclerosis. The demonstration of characteristic cholesterol crystals in tissue biopsy specimens is a pathognomonic finding. However, renal cholesterol embolism may be clinically diagnosed when renal failure develops after known inciting factors or together with systemic manifestations of atheromatous embolization such as lower extremity livedo reticularis, focal digital ischemia or retinal embolism. Previous investigators have emphasized the progressive nature of renal insufficiency due to cholesterol embolism, its poor prognostic significance and almost uniformly fatal outcome. In this report, we describe five additional patients with renal cholesterol embolization. In three of them only moderate renal insufficiency developed, and kidney function subsequently improved in all. In two patients the condition progressed to end-stage renal disease; one died with chronic renal failure whereas the other patient required four months of hemodialysis before kidney function eventually improved. Thus, cholesterol embolization may produce a spectrum of renal functional impairment. In some patients there is only a moderate loss of renal function with subsequent improvement; in others renal failure ensues. In this latter group, eventual return of kidney function can occur even after a prolonged period of renal insufficiency.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
7/11. The pathophysiologic role of fat in dysbaric osteonecrosis.Dysbaric osteonecrosis (DON) can occur in humans and sheep after a single hyperbaric air exposure with inadequate decompression. The authors hypothesize that DON does not result from primary embolic or compressive effects of nitrogen bubbles on the osseous vasculature, but by secondary injury to the marrow adipose tissue by rapidly expanding nitrogen gas that triggers local, and possibly systemic, intravascular coagulation. A 28-year-old scallop diver remained at a depth of 92 feet in sea water for 4.5 hours on surface-supplied compressed air. decompression sickness occurred after a no-stop ascent to the surface, and he died 70 minutes later. autopsy showed multiple gas bubbles, not only within the great vessels, but in the fatty marrow of his femoral and humeral heads. Lipid and platelet aggregates were found on the surface of marrow bubbles. Fibrin-platelet thrombi were detected within dilated venous sinusoids adjacent to bubbles, and in veins, capillaries, and arterioles. Since pulmonary, renal, and intraosseous (subchondral) fat embolism and fibrin thromboses were observed, it is suggested that injured marrow adipocytes can release liquid fat, thromboplastin, and other vasoactive substances, which conceivably can also play a systemic procoagulant role in triggering disseminated intravascular coagulation and additional DON.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
8/11. Fat embolism, intravascular coagulation, and osteonecrosis.A triad of intraosseous fat embolism, intravascular coagulation (both thrombosis and hemorrhage), and osteonecrosis was pathologically demonstrated to coexist for the first time in humans. Specimens were evaluated from the earliest nontraumatic (18 hours) and traumatic (29 hours) femoral head lesions yet reported, and the cause and early pathogenesis were confirmed in a third case. An absolute overload of subchondral fat emboli, with hypercoagulability, stasis, and endothelial damage by free fatty acids, appears to cause end-organ death by triggering intravascular coagulation. This intermediary pathway appears to be capable of producing osteonecrosis by progressive fibrin platelet thromboses, which begin in vulnerable subchondral capillaries and sinusoids, especially when associated with arteriolar vasoconstriction and impaired secondary fibrinolysis (reperfusion of necrotic vessels with peripheral marrow hemorrhages). A relative overload of subperiosteal and subchondral fat emboli, which is below the ischemic/anoxic threshold but insufficient for intravascular coagulation, may cause osteopenia.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
9/11. Autologous fat injection for soft tissue augmentation in the face: a safe procedure?Autologous fat injection for soft tissue augmentation in the face is claimed to be a safe procedure. However, there are several case reports in the literature where patients have suffered from acute visual loss and cerebral infarction following fat injections into the face. Acute visual loss after injection of various substances into the face is a well-known complication of such interventions. We report two further patients who suffered from ocular and cerebral embolism after fat injections into the face. For the intravasation of fat particles there are three preconditions: well-vascularized tissue, fragmentation of parenchyma, and, especially, a local increase in pressure in the affected tissue. Fat injections into the face lead to an acute local increase in pressure in highly vascularized tissue. We assume that fragments of fatty tissue reach ocular and cerebral arteries by reversed flow through branches of the carotid arteries after they are introduced into facial vessels. The manifestation of fat embolism appears either immediately after the fat injection or after a latency period. Fat embolism can remain subclinical and may not be recognized, or the clinical features may be misinterpreted. To minimize the risk of such a major complication, fat injections should be performed slowly, with the lowest possible force. One should avoid fat injections into pretraumatized soft tissue, for example, after rhytidectomy, because the risk of intravasation of fat particles may be higher. Metabolic disturbances such as hyperlipidemia may also contribute to the clinical manifestation of fat embolism Routine funduscopic examinations after fat injections into the face could help to provide data for future estimation of the patient's general risk.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
10/11. Evaluation of acute mental status change in the nonhead injured trauma patient.Acute mental status change in the first 24 hours after trauma is uncommon in nonhead injured patients who initially present with a normal sensorium. Although arterial hypoxemia is the classic etiology for such a mental status change, three less common etiologies should always be considered: cerebral fat embolism, blunt carotid artery injury, and vertebrobasilar artery thrombosis. Prompt diagnosis and appropriate treatment can significantly improve patient morbidity and mortality. Three nonhead injured trauma patients are described illustrating cerebral fat embolism, blunt carotid artery injury, and vertebrobasilar artery thrombosis as causes of acute mental status change. Each patient initially presented with a clear sensorium, but subsequently developed neurological deficits within 24 hours after admission. All had a normal admission CT scan of the head. MRI or conventional arteriography was diagnostic in each case. Any patient who is initially lucid and subsequently develops a neurological deficit, or a patient whose neurological status does not correlate with brain CT findings should undergo immediate evaluation for possible cerebral fat embolism or cervical vessel injury. An algorithm for management of nonhead injured trauma patients with acute mental status deterioration is presented.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
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