Preventing postoperative thromboembolism.
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Biomedical subjects
Publications and source records attributed to G McGarrity.
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Desmoid tumours are not common but have a distinct resemblance to fibrosarcomata. Their clinical appearance and progress should be recognised since failure to distinguish them from sarcomata could result in extensive and unnecessarily mutilating operations. Three cases of extra-abdominal desmoid tumours are reported. Two of the patients had tumours arising from multicentric foci in the same limb. The disappearance of the tumours in two patients after the menopause, and the variation in the tumours during the menstrual cycle in the third patient, add weight to the theories about endocrine control.
The fibrinogen uptake test has been used to detect deep vein thrombosis after total hip replacement in 90 patients. The upper third of the thigh in each leg was ignored and peripheral leg counting carried out distal to this. The results were directly compared with the findings of venography in the 170 legs of the 90 patients. There was a high false positive rate (30 per cent) with the fibrinogen uptake test which was associated with the presence of the knee joint effusion or varicose veins, but not with the site of operation. There was a low false negative rate (less than 5 per cent), and the fibrinogen uptake test, used in this way, may fail to detect a percentage of small thrombi in the wound area that are probably produced by the local trauma of operation. It is considered that the fibrinogen uptake test has a clinical use as a screening test for deep vein thrombosis after hip replacement, but venography is required in the interests of accuracy.
The effect of an angiotensin-converting enzyme inhibitor on the circulating levels of angiotensin I, angiotensin II, and arginine vasopressin was studied in dogs subjected to hypotensive hemorrhagic shock. In dogs subjected to hemorrhage but not given the inhibitor, angiotensin II rose 20-fold (from 69 to 1,343 pg/ml of plasma), whereas in dogs subjected to hemorrhage but pretreated with the inhibitor, angiotensin II rose only 2-fold (from 92 to 171 pg/ml of plasma). In the pretreated dogs angiotensin I rose 30-fold (from 108 to 3,232 pg/ml of plasma). There was no statistically significant difference between the vasopressin levels found in the untreated dogs and the levels found in dogs given the inhibitor (1,016 and 1,095 pg/ml of plasma). Of the 15 dogs in the untreated group, five died before retransfusion was completed (four of cardiac failure and one of cardiac arrhythmia); none of the 10 dogs in the inhibitor-treated group died. These observations suggest that the very high levels of angiotensin II observed following severe hemorrhage do not contribute significantly to the increased secretion of vasopressin and that the inhibitor protects against death, possibly by suppressing the very high blood levels of angiotensin II observed following this type of experimental hemorrhagic shock.
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