Late massive haemoptyses from bronchopulmonary collaterals in infarcted segments following pulmonary embolism.
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Massive, recurrent haemoptyses requiring blood transfusions occurred in a patient who had been diagnosed as having pulmonary thromboembolism 3 months earlier. To the authors' knowledge this is the first case report of this kind, in which massive haemoptyses were proved to be caused by large bronchopulmonary collaterals that had developed in the infarcted lung segments affected by embolism. Selective embolization of the collaterals proved to be therapeutic and life saving. (+info)
Necrosis correlates with high vascular density and focal macrophage infiltration in invasive carcinoma of the breast.
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Necrosis is a common feature of invasive carcinoma of the breast and is caused by chronic ischaemia leading to infarction. Although necrosis was previously assumed to be due to a generally poor blood supply in the tumour, in this study we show that it is present in tumours with focal areas of high vascular density situated away from the actual sites of necrosis. This may account, in part, for the previous observation that necrosis is linked to poor prognosis in this disease. Highly angiogenic tumours often display blood vessel shunting from one tumour area to another, which further exacerbates ischaemia and the formation of tumour necrosis. We have recently demonstrated that high focal microphage infiltration into breast tumours is significantly associated with increased tumour angiogenesis and poor prognosis and that the macrophages accumulate in poorly vascularized, hypoxic areas within breast tumours. In order to investigate the interactions of macrophages with chronic ischaemia (as reflected by the presence of necrosis) and angiogenesis in breast tumours, we quantified the levels of these three biological parameters in a series of 109 consecutive invasive breast carcinomas. We found that the degree of tumour necrosis was correlated with both microphage infiltration (Mann-Whitney U, P-value = 0.0009; chi-square, P-value = 0.01) and angiogenesis (Mann-Whitney U P-value = 0.0008, chi square P-value = 0.03). It was also observed that necrosis was a feature of tumours possessing an aggressive phenotype, i.e. high tumour grade (chi-square, P-value < 0.001), larger size (Mann-Whitney U, P-value = 0.003) and low oestrogen receptor status (Mann-Whitney U, P-value = 0.008; chi-square, P-value < 0.008). We suggest, therefore, that aggressive tumours rapidly outgrow their vascular supply in certain areas, leading to areas of prolonged hypoxia within the tumour and, subsequently, to necrosis. This, in turn, may attract macrophages into the tumour, which then contribute to the angiogenic process, giving rise to an association between high levels of angiogenesis and extensive necrosis. (+info)
Cluster headache-like attack as an opening symptom of a unilateral infarction of the cervical cord: persistent anaesthesia and dysaesthesia to cold stimuli.
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A 54 year old man experienced excruciating left retro-orbital pain with lacrimation and redness of the eye representative of a cluster headache attack. This was followed by left hemiparesis with plegia of the lower limb and left Horner's syndrome. Five days later the hemiparesis recovered while the patient developed hypoanaesthesia to cold stimuli that evoked painful burning dysaesthesia on the right side below the C4 level. MRI disclosed a discrete infarct in the left lateral aspect of the cord at C2 level concomitant to a left vertebral artery thrombosis. This limited infarct and the clinical symptoms suggest a hypoperfusion in the peripheral arterial system of the left hemicord, supplied both by the anterior and posterior spinal arteries. Cluster headache-like attack and persistent dysaesthesia to cold stimuli are discussed respectively in view of the central sympathetic involvement and partial spinothalamic system dysfunction. (+info)
Thromboatheromatous complications of umbilical arterial catheterization in the newborn period. Clinicopathological study.
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Severe catheter-related thromboatheromatous lesions were found at necropsy in 33 of 56 infants who had umbilical arterial catheters passed during life. In infants dying within 8 days of insertion of the catheter, varying degrees of thrombosis of the aorta and its major branches were seen. With increasing thrombosis and aging of the thrombus, fatty deposits were seen first within the thrombus, and then in the intima and media. In addition there was evidence of proliferation of medial smooth muscle cells and of disruption of the medial architecture below the thrombus, characterized by the presence of abundant mucopolysaccharide. In infants who survived longer, varying degrees of organization of the thrombus could be traced, leading eventually to raised fibrous plaques with lipid and occasionally calcification. The lesions in the older infants were similar in many respects to experimental thromboatheromatous lesions produced in rabbits, and to some lesions of artheroma occurring spontaneously in humans. A wide variety of embolic phenomena were found, with features suggesting asynchrony of embolic episodes. The presence of thrombotic lesions could not be related to birthweight, Apgar scores at 1 and 5 minutes, age at catheterization, duration of catheterization, underlying disease process, age at death or the presence of hypothermia, acidosis, or anomalies in coagulation tests. There is a need for less hazardous methods of monitoring arterial oxygen tension. (+info)
The pathogenesis of Perthes' disease.
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It has been shown that in the puppy, two infarcts separated by an interval of four weeks produce a disorder of long duration which results in flattening and broadening of the femoral head and which reproduces the radiological changes seen in Perthes' disease in man. The histological appearances produced by two infarcts are characteristic. In this study the histological appearance of fifty-seven femoral head biopsy specimens in Perthes' disease in man have been studied. In 51 per cent of hips histopathological changes characteristic of double infarction were present, and there were grounds for postulating that double infarction might eventually occur in all cases. The findings support the concept that the deformation of the femoral head and the chronicity of Perthes' disease in man may be due at least as much or even more to repeated episodes of infarction and the ensuing abnormalities of growth as to mechanical factors related to weight-bearing. (+info)
Clinical and radiological aspects of idiopathic diabetic muscle infarction. Rational approach to diagnosis and treatment.
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The systemic effects of diabetes mellitus are well recognised. The heart, kidney, central and peripheral nervous systems, and the distal parts of the limbs are often the site of end-organ damage resulting from ischaemia. Infarction of large muscle groups in the limb, not associated with gangrene, is uncommon. There have been few reported cases other than radiological descriptions of diabetic muscle infarcts. While previous reports have illustrated some of the clinical and radiological characteristics of this condition, the paucity of published cases makes it difficult to determine the most appropriate methods of diagnosis and treatment. During a five-year period we treated 14 patients with diabetes mellitus, aged from 32 to 59 years, who were referred to a musculoskeletal oncology service for suspected soft-tissue sarcoma, but were subsequently found to have a diabetic muscle infarct. Closed needle biopsy was performed in 13 without complications. In 12 patients, the symptoms resolved without surgical treatment. (+info)
Disseminated thrombosis and bone infarction in female rats following inhalation exposure to 2-butoxyethanol.
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Groups of 10 male and 10 female F344/N rats were exposed to 0, 31, 62.5, 125, 250, and 500 ppm of 2-butoxyethanol (BE) by inhalation, 6 hr/day, 5 days/wk, for 13 wk. Four moribund female rats from the 500 ppm group were sacrificed during the first 4 days of exposure, and 1 moribund female from the same group was sacrificed during week 5. Dark irregular mottling and/or loss of the distal tail were noted in sacrificed moribund rats. Similar gross lesions were noted in the terminally sacrificed females exposed to 500 ppm BE. Histologic changes noted in the day 4 sacrificed moribund rats included disseminated thrombosis involving the coccygeal vertebrae, cardiac atrium, lungs, liver, pulp of the incisor teeth, and the submucosa of the anterior section of the nasal cavity. Alterations noted in coccygeal vertebrae from the 500 ppm sacrificed moribund rats included ischemic necrosis and/or degeneration of bone marrow cells, bone-lining cells, osteocytes (within cortical and trabecular bone), and chondrocytes (both articular and growth plate), changes that are consistent with an infarction process. The moribund female rat that was sacrificed during week 5 and those female rats treated with 500 ppm and sacrificed following 13 wk of treatment lacked thrombi, but they had coccygeal vertebral changes consistent with prior infarction and transient or complete bone growth arrest. No bone lesions or thrombi were noted in the male rats treated with the same doses of BE. In conclusion, exposure to 500 ppm BE vapors caused acute disseminated thrombosis and bone infarction in female rats. Possible pathogenic mechanisms are discussed. (+info)
The course of the remnant kidney model in mice.
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The remnant kidney model was produced in mice by unilateral nephrectomy and partial infarction of the remaining kidney. Control mice underwent laparotomy only. The mice were studied for up to 44 weeks. No quantitative differences were noted in systolic arterial pressure, proteinuria, or histopathology between control mice and those with a remnant kidney. Glomerular enlargement occurred in the remnant kidney. (+info)