D. J. du Plessis Lecture. Surgical research--does the patient benefit? Presented at the Surgical Research Society of Southern Africa meeting, Bloemfontein, 28-29 July 1999.
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Biomedical subjects
Publications and source records attributed to L J Levien.
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PURPOSE: This report summarizes our experience with the popliteal entrapment syndrome in 88 limbs (48 patients) treated during a 10-year period. METHOD: The study cohort consisted of a retrospective analysis of those patients who were seen with symptoms of claudication or severe ischemia by a single surgical group and in whom unequivocal evidence of popliteal entrapment was shown either with angiography or at the time of operation. The cases were collected prospectively in a private vascular surgical practice. RESULTS: Bilateral popliteal entrapment was found in 40 of the 48 patients. The mean age at the time of presentation was 35.0 years (SD, 11.6 years). Claudication was the most frequent presenting symptom (70 of 88 limbs). Types I, II, III, and IV popliteal entrapment were found in 58 limbs (15 arteries occluded), and 30 limbs (three occlusions) were seen with a "functional" popliteal artery entrapment (apparent absence of a developmental anatomic abnormality). Of the 18 limbs with severe ischemia and associated occlusion of the popliteal artery, 15 underwent bypass grafting with reversed saphenous vein grafts, all of which remained patent during the follow-up period (median follow-up, 4.2 years; range, 1 to 10 years). One popliteal artery occlusion that was treated with thrombectomy and vein patching occluded within 6 months and necessitated subsequent vein grafting. Two limbs with inoperable occluded popliteal arteries were not subjected to reconstruction (one necessitated amputation because of advanced ischemia, and the second had extensive thrombosis of the distal run-off). In two patients (four limbs), moderate presenting symptoms abated without surgery after the discontinuation of an extreme exercise program. The remaining limbs underwent surgical decompression (all popliteal arteries remained patent, with a median follow-up of 3.9 years). CONCLUSION: The popliteal entrapment syndrome is more prevalent than has formerly been appreciated. On the basis of observations made in this series and in the surgical literature, we advise surgical correction in all cases of types I, II, III, and IV entrapment at the time of diagnosis to avoid occlusion as a result of continued arterial wall degeneration. In contrast, decompression is only advised in those patients with "functional entrapment" if they have discrete and typical symptoms because up to 50% of the normal population may display transient popliteal artery compression with extremes of plantar flexion or dorsiflexion. On the basis of the severe histologic changes found in those popliteal arteries that had undergone occlusion at the time of presentation, it is advised that the popliteal artery should be completely replaced, ideally with a vein graft, when significant degeneration or occlusion of the popliteal artery is noted at the time of operation.
PURPOSE: Six cases of adventitial cystic disease were studied, and the existing theories of the aetiology of adventitial cystic disease were reviewed to present evidence in support of a variation of the developmental hypothesis that might explain the sites of occurrence of this rare condition. METHODS: Cases of adventitial cystic disease were collected by interrogation of the records of a group of vascular surgeons in the Johannesburg area. After reviewing the relevant literature, the sites of occurrence of 323 cases of adventitial cystic disease were documented, and the theories of the formation of adventitial cystic disease were reviewed. The embryological origin of those vessels in which adventitial cystic disease occurs was investigated. Clinical cases were collected in private practice vascular referral centers. The clinical features, treatment, and subsequent course of six cases of adventitial cystic disease (four related to the popliteal artery, one in the femoral artery, and one in the radial artery) are included. RESULTS: All cases of adventitial cystic disease reported have occurred in the nonaxial arteries, which form at a later stage than the axial vessels during limb differentiation and development. It is therefore postulated that during limb bud development cell rests derived from condensations of mesenchymal tissue destined to form the knee, hip, wrist, or ankle joints are incorporated into the nearby and adjacent nonaxial vessels during development of these vessels in the 15-22-week stage. These newly forming nonaxial vessels develop from vascular plexuses during the same stage of development, and in close proximity to the adjacent condensing joint structures. It is further postulated that these cell rests are then responsible for the formation of adventitial cystic disease later in life, when the mucoid material secreted results in a mass lesion within the arterial or venous wall. CONCLUSION: There is evidence supporting the hypothesis that adventitial cystic disease is a developmental condition occurring in the nonaxial blood vessels.
OBJECTIVES: This study was performed to demonstrate the value and durability of intraoperative retrograde angioplasty for stenotic lesions of the aortic arch branches at the time of carotid endarterectomy for the treatment of tandem proximal and bifurcation carotid lesions. DESIGN: Retrospective analysis of the clinical data. METHODS: Forty-four patients were included in this study when they presented with symptomatic extracranial vascular disease due to stenosis of both a proximal aortic arch branch and carotid bifurcation disease. Tandem disease was detected in the vascular laboratory and confirmed by angiography. Each patient was subjected to conventional carotid endarterectomy, and at the time of operation, the proximal lesion was subjected to transluminal angioplasty through the endarterectomy arteriotomy (brachiocephalic 24; left common carotid 15; right common carotid artery five). Patients were then followed up clinically and by non-invasive tests at 6-monthly intervals. RESULTS: Forty-three successful dilatations were achieved. The single initial technical failure was due to heavy calcification of a brachiocephalic artery. In the follow-up period restenosis was noted in four patients. All restenosis occurred within 24 months. No restenosis at the angioplasty site was noted on subsequent follow-up of the remaining 39 patients. No perioperative stroke or death was encountered. A surprisingly high mortality rate was noted on follow-up in this group of patients, suggesting the presence of more aggressive and advanced diffuse vascular disease. CONCLUSION: Retrograde intraoperative angioplasty of the proximal component of a tandem extracranial lesion has in this series proven to be a safe and durable therapeutic option. This technique has an acceptable restenosis rate in a subset of patients who have been demonstrated to have a shortened life expectancy and a high mortality rate in the follow-up period.
We describe a series of experiments in which a subhuman primate model was used to create temporary and permanent cerebral ischemia by three separate mechanisms. In the first group of five baboons, a hemodynamic model was produced by creating unilateral and bilateral carotid stenotic lesions of varying degrees with and without associated reduction in systemic perfusion pressure. Only global ischemic changes and no focal changes resulted. In the second group of three baboons, a macroembolic model was produced by introducing solid particulate material into the extracranial circulation. No reversible contralateral focal neurologic changes resulted. In the third group of 11 baboons, cerebral ischemia was produced by introducing agents known to cause platelet aggregation (arachidonic acid, adenosine diphosphate, and collagen) into the extracranial arterial circulation. Arachidonic acid caused seizures, adenosine diphosphate caused severe postural hypotension, and only collagen fibrils produced a picture resembling a transient ischemic attack. We propose a theory that intravascular activation of the prostaglandin cascade by chemical initiation may result in the pathophysiologic changes of transient cerebral ischemia.
This study evaluates whether medical therapy alone can achieve satisfactory results in the treatment of low grade carotid stenosis or ulcerated plaques. Out of 525 patients presenting with transient or minor strokes, 64 were found with unilateral extracranial vascular disease as the sole potential source for their neurological symptoms. Utilizing arteriographic criteria, 35 patients with ulcerated plaques or carotid artery stenosis of less than 50% luminal artery diameter were treated conservatively with aspirin and dipyridamole (300 mg/day each). Twenty-nine patients with unilateral internal carotid artery stenosis of greater than 50% luminal artery diameter were treated by means of carotid endarterectomy. Follow-up in the two groups for a mean period of 24-26 months revealed no major strokes or neurological deaths in either group. Myocardial infarction was the major cause of death. Two patients developed subsequent transient ischemic attacks, and one a minor stroke with total recovery in the conservatively treated group. All became asymptomatic when warfarin replaced aspirin therapy. The findings in this study confirmed that "low grade" stenoses can be safely treated by medical measures alone.
This study examined the hypothesis that diabetes mellitus predisposes the brain to irreversible ischaemic damage rather than to reversible transient ischaemic attacks. Of 525 patients presenting with transient or minor strokes, 54 patients were found to have diabetes mellitus and 471 patients had no evidence of diabetes. The diabetic subgroup was significantly more hypertensive than the non-diabetic subgroup (P less than 0.001). In an overall comparison of the prevalence of strokes and transient ischaemic attacks in diabetic and non-diabetic subgroups, 26 (6.7%) of 388 patients with transient ischaemic attacks had diabetes mellitus, and 362 (93.3%) of 388 patients with transient ischaemic attacks were non-diabetic. Thus diabetes was not a significant risk factor for TIAs (P less than 0.001). However when the role of diabetes in causing strokes was assessed in all 525 patients evaluated in the study, 28 of 54 diabetics presented with strokes whereas 109 of 471 non-diabetics presented with strokes. Statistically diabetics were 3-4 times more likely to present with a stroke than non-diabetics (P less than 0.0001) in keeping with the findings in other centres. The findings of this study appear to support the hypothesis that diabetics are at a greater risk of permanent cerebral ischaemia without prior warning of a transient ischaemic event than their non-diabetic counterparts. It may be advisable to screen asymptomatic diabetic patients aggressively and to consider these patients as a high risk subgroup for potential stroke if extracranial carotid vascular disease is present.
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Two patients in whom asymptomatic and small hepatocellular carcinomas (HCC) were detected by alpha-fetoprotein (AFP) screening are reported. Both patients were hepatitis B surface antigen-positive. In the first patient, the tumour grew slowly and was resected more than 2 years after a significant elevation in serum AFP levels had been first detected and 13 months after hepatic angiography confirmed the presence of a vascular tumour. In the second patient, a small encapsulated HCC was diagnosed by AFP screening and hepatic imaging. The clinical course in these 2 patients illustrates that small, asymptomatic and encapsulated HCCs do occur in southern African black hepatitis B carriers. Regular screening of patients at risk may be justified.
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Seven cases of fibromuscular dysplasia of the carotid artery are presented. Six of these patients presented with transient or fixed neurological deficit and 1 with intracranial haemorrhage. The uncertainty about the natural history of this condition is highlighted, and guidelines to the management of symptomatic patients as well as the more controversial incidentally diagnosed asymptomatic patient are outlined. A novel form of intra-operative use of a Grunzig balloon dilatation catheter in the management of fibromuscular dysplasia is presented.
In the presence of internal carotid artery occlusion, external carotid artery disease can produce neurological symptoms either by reducing flow in the collateral vessels to the circle of Willis, or by acting as a source for embolic disease. Five cases are described to illustrate the clinical presentations possible in this situation, and to demonstrate the symptomatic relief afforded by correctly selected external carotid endarterectomy.
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A combination of non-invasive tests consisting of Doppler ultrasound carotid velocity assessment, carotid phono-angiography and directional Doppler supra-orbital flow evaluation was used to detect internal carotid stenosis of 50% or more in patients with symptoms suggestive of cerebrovascular disease. When compared with contrast arteriography in 75 carotid arteries this battery of non-invasive tests detected 18 of 19 cases of carotid stenosis, resulting in a sensitivity of 95%. Three false-positive results yielded a specificity of 95%. The accuracy achieved with this non-invasive battery of tests suggested that clinical decisions are warranted on the basis of their results.
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Five hundred patients referred to the Cerebrovascular Clinic of the Johannesburg Hospital were examined by a battery of noninvasive tests and angiography. Thirty four occlusions of the internal carotid artery were found in 32 patients. These patients were prospectively evaluated, including clinical examination, analysis of risk factors and subsequent management. This group of patients was followed up for a mean period of 18 months, and the clinical and laboratory findings and follow up data of this group were compared to an age and sex matched group of patients with matched presenting symptoms, but with patent internal carotid arteries on angiography. Four clinical patterns emerged in the patients with occluded carotid arteries; asymptomatic (3), TIA's (17), initial fixed stroke (7), and TIA with subsequent stroke (5). Follow up of the occluded group revealed 19 patients (59%) with no further symptoms and no indication for surgical intervention. Nine patients required surgery; 4 external carotid endarterectomies (ipsilateral), 4 internal carotid endarterectomies (contralateral), and one extracranial to intracranial bypass. Two were lost to follow up and one died. After 18 months mean follow up 29 patients (91%) were well and asymptomatic. Follow up for a similar period of the non-occluded group revealed three deaths, three late strokes and three myocardial infarctions. None were lost to follow up. After 19 months mean follow up 26 patients (81%) were well with no new neurological symptoms. The prognosis of appropriately treated patients with total occlusion of the internal carotid artery does not appear to be worse than in patients with similar presenting features and patent carotid arteries.(ABSTRACT TRUNCATED AT 250 WORDS)