Biomedical subjects

R S Lord

Publications and source records attributed to R S Lord.

151 records · Page 9Linked to original sources

PubMedDate not supplied

Thoracoabdominal aortic aneurysm reconstruction.

Thoracoabdominal aortic reconstruction distal to the left subclavian artery was carried out on 19 patients between 1974 and 1990. Screening procedures to detect cardiac, respiratory or renal impairment were undertaken in all patients. Reconstruction was in the upper third of the descending aorta in 6 patients, middle third in 6 patients, and lower third in 7 patients. The Crawford inclusion technique was used in all cases. There were six deaths, four of which were from the high reconstruction group, and one each from the middle and lower group. Paraparesis occurred in 4 patients, 2 of whom survived with some impairment. Temporary renal failure was seen in 2 patients, liver failure in 2, respiratory failure in 2, sepsis in 1, myocardial infarction in 1, and severe coagulopathy in 3. The perioperative mortality rate was 32% for the group as a whole and 15% for reconstructions which started at the middle or lower thoracic level. We conclude that the mortality rate for the middle and lower reconstructions is acceptable but that alternative techniques for the high aneurysms should be sought.

Anastomosis, Surgical↗

PubMedDate not supplied

Acute aortic occlusion presenting with lower limb paralysis.

In a two year period eight patients have presented with acute aortic occlusion and a poor outcome in seven. Initial failure to diagnose aortic occlusion, with a mean delay from presentation to diagnosis of 24 hours, was mainly responsible. All patients had varying degrees of paralysis on presentation which misled clinicians although other findings of acute ischaemia (pain, absent pulses, colour change and anaesthesia) were always present. Two patients were initially referred to a neurologist, another to a neurosurgeon, and the fourth to an orthopaedic surgeon. Even after diagnosis had been established, the need for urgent revascularization was not always recognized, the mean time from diagnosis to revascularization being 13 hours. Unnecessary aortography contributed to this delay in four patients. In two patients operative treatment was not undertaken while six were treated operatively by: aortic bifurcation graft (3), aortic thromboendarterectomy and femoropopliteal bypass (1), open aortic embolectomy (1) and bilateral femoral embolectomy (1). The causes of aortic occlusion were thrombosis of an atherosclerotic aorta (5), thrombosis of an aneurysm (2) and embolism (1). In the latter patient, the heparin induced thrombocytopenia syndrome (HITS) was primarily responsible. The outcomes in the eight patients were death (5), paraplegia (1), amputation (1), and uncomplicated recovery (1). The single patient who made an uncomplicated recovery had the shortest delay from presentation to revascularization of only 2 1/4 hours. Acute aortic occlusion rivals aortic rupture as a vascular emergency and demands immediate operative intervention.

Acute Disease↗

PubMedDate not supplied

Radiologic control of operative carotid dilatation. Aneurysm formation following balloon dilatation.

Dilatation of the dysplastic internal carotid artery has been controlled by intraoperative radiography including angiography. The method minimizes the risk of damaging the artery at the base of the skull while allowing immediate visualisation of the results. In one case persisting stenosis after passage of a metal dilator was treated by balloon dilatation with the formation of a localised aneurysm.

Aneurysm↗

PubMedDate not supplied

Symptomatic carotid restenosis.

Between May, 1969, and December, 1985, 680 carotid endarterectomies were carried out in the Surgical Professorial Unit in St. Vincent's Hospital, Sydney. Recurrence requiring re-operation was detected in nine arteries in seven patients. Continued smoking after the initial operation may have contributed to the restenoses. The origin of the internal carotid artery was the most common site of recurrence, irrespective of whether restenosis was caused by myointimal fibroplasia or recurrent atheroma.

Arterial Occlusive Diseases↗

PubMedDate not supplied

The acute response of indium-111 labelled platelets to arteriotomy closure.

A standard 40 mm arteriotomy was created in canine iliac and carotid arteries and then closed by either direct suture without a patch, with a vein patch or with a polytetrafluoroethylene patch (PTFE). The uptake of 111-Indium oxine labelled platelets at 2 hours after operation was compared between the groups. Arteriotomies closed with a PTFE patch demonstrated significantly greater platelet aggregation than those closed with a vein patch. Primary closure without a patch was associated with the least platelet uptake of all (PTFE versus vein patch, P less than 0.01; PTFE versus no patch, P less than 0.01; vein patch versus no patch, P less than 0.05). Light and electron microscopy confirmed the radioisotopic findings.

Animals↗

PubMedDate not supplied

Cerebral perfusion defects, dysautoregulation and carotid stenosis.

Single Photon Emission Computed Tomography (SPECT), imaging of cerebral blood flow was carried out in ten patients with haemodynamically significant carotid stenosis. Before and after carotid endarterectomy each patient was investigated by 3--dimensional SPECT brain scanning using technetium--hexamethyl propyleneamine oxine (99 mTcHMPAO, ceretec). Brain blood flow was normal before and after operation in 3 patients whose autoregulation was kept intact. Seven patients received acetazolamide to limit cerebral vascular reactivity and in four of these, preoperative perfusion defects were visible. After carotid endarterectomy the ipsilateral perfusion defects were abolished and it is concluded that carotid stenosis can reduce perfusion in the dysautoregulation brain and that carotid reconstruction can restore normal flow.

Acetazolamide↗

PubMedDate not supplied

Cell death in atheromatous plaque of the carotid artery occurs through necrosis rather than apoptosis.

Thrombogenic plaques associated with acute myocardial infarction and sudden cardiac death are relatively acellular but the mechanisms responsible for cell loss are uncertain. To help elucidate this, we investigated advanced atherosclerotic lesions taken from 13 carotid arteries. The number of cells detected by the technique for identifying DNA fragmentation (occurring at apoptosis and necrosis) known as terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) technique varied in arteries from 9.6% to 40.3% and was 4 times higher in plaque (26.4 +/- 2.9%) than in the adjacent media (6.0 +/- 1.3%). The majority of TUNEL+ cells (75.5 +/- 5.6%) were smooth muscle cells (SMCs) as they also reacted with antibodies to SMC alpha-actin and myosin. TUNEL+ nuclei were found in macrophages (CD68+ cells), T-cells (CD3+ cells) and neovascular endothelial cells (von Willebrand factor: vWf+ cells) as well. From 13.0% to 34.0% (24.6 +/- 1.7%) of plaque cells stained with antibody to proliferating cell nuclear antigen (PCNA) whereas the number of PNCA+ nuclei in the adjacent media was 6 times lower (4.1 +/- 0.7%). In plaques, the number of PCNA+ cells correlated with the number of TUNEL+ cells (r = .66; p < .001) but the proportion of PCNA+ SMCs was relatively low (39.1 +/- 5.2%). Electronmicroscopic examination showed the presence of cells with condensed chromatin and convoluted cell surfaces in all arteries tested and the numbers of cells exhibiting these destructive alterations varied from 15.2% to 35.5% but no cells with typical expression of apoptotic death were detected. The results obtained indicate that all vascular cell types undergo cell death, with some prevalence in locations close to the plaque core and that intimal cells die through necrosis rather than apoptosis. We speculate that the imbalance in SMC death and proliferation may lead to acellular plaque formation.

Apoptosis↗