[Aneurysms of the peripheral arteries. II. Aneurysms of the upper limbs].
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Biomedical subjects
Publications and source records attributed to R Limet.
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A 73-year-old man was admitted for rupture of an atherosclerotic aneurysm of the profunda femoris artery associated to popliteal and bilateral axillary arteries aneurysms. The aneurysm of the profunda femoris artery was developed between the branches of the crural nerves. Considering the patency of the superficial femoral artery and of the leg arterie, and to avoid injury to the crural nerve, no reconstruction of the profunda femoris was attempted. The aneurysm was ligated proximally and buttress sutures were placed on the site of rupture to achieve thrombosis of the aneurysms. Most of the published cases of aneurysm of the profunda femoris artery are false aneurysms developed after various trauma. Atherosclerotic aneurysm of the profunda femoris artery is a rare lesion and rupture is exceptional.
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Two cases of life-threatening haematuria, secondary to an uretero-arterial fistula, are reported. Both cases present predisposing causative factors. One patient had a combination of previous aorto-bifemoral bypass grafting, an iliac artery aneurysm (retrogradely perfused), and an indwelling ureteral stent for ureteral compression. The other patient had previous aortoiliac surgery and obstructive uropathy with chronic urinary tract infection. Preoperative diagnosis of uretero-arterial fistula was made in only one patient. He was successfully operated (exclusion of the iliac aneurysm). In the other patient, nephrectomy was attempted to control reno-ureteral bleeding of unknown origin. Fatal recidive of brisk haematuria occurred some days later. Factors contributing to the development of uretero-arterial fistula, their diagnosis and optimal treatment are discussed.
A case of type III aortic dissection which occurred fourteen months after heart transplantation is presented. Medical therapy was instituted to achieve controlled hypotension. The evolution was favorable and the patient could be discharged after one month. Hypertension and increased ejection fraction after transplantation could have been predisposing factors via an increase of the shear stress in the aorta.
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From January 1993 to December 1995, intraarterial catheter guided urokinase infusion was used as an initial approach in the management of 29 episodes of infrainguinal graft thrombosis (12 venous and 17 prosthetic grafts) in 27 patients. The infusion catheter was embedded inside the occluding clot which was infiltrated by 225.000 U urokinase from distal to proximal. Local low-dose urokinase (1.000 U/kg/hr) was continued for a mean of 39 hours. By this regimen, prompt relief of ischaemia was achieved in 69% (20/29) of cases. Complete recanalization was obtained in 79% of cases. In six cases, the graft remained totally (n = 3) or partially (n = 3) occluded. Two of these patients benefited from secondary surgery, two improved clinically by conservative treatment, and two required amputation. In the 23 successful cases, thrombolysis unmasked an underlying flow-limiting stenosis in 83% (19/23), that was subsequently corrected by percutaneous balloon angioplasty (n = 15), by surgery (n = 3), or by a combination of both (n = 4). One early rethrombosis resulted in an amputation. The immediate limb-salvage rate was 89% (26/29). Surgical intervention was avoided in 17 cases (58%). The main hospital stay was 13 days. The short-term follow-up (mean of 17 months) reveals a high early rethrombosis rate (8/23 or 35%) within one year. Four of these repeated graft failures evolved to amputation. At one year, the overall limb salvage rate dropped to 79%. Thrombolytic management of infrainguinal occluded bypass grafts gives excellent initial technical results (79%), minimizing the need for major surgical revision. It is however characterized by a high procedure-related morbidity (21%). These immediate favourable results are not longstanding. Diffuse graft disease, limited outflow and high recurrence rate of anastomotic stenoses after balloon angioplasty explain poor long-term results after thrombolysis of failed grafts.
The medical records of nine patients (five female and four male, mean age 58 +/- 5 years) presenting with a carotid chemodectoma between 1983 and 1995 were reviewed. In two cases (22%) the diagnostic was not suspected at the time of initial presentation. The most common complaint was a swelling in the anterolateral region of the neck. One patient (11%) presented with a preoperative peripheral nerves deficits (vagus and hypoglossal palsies and Horner's syndrome). Two tumours were embolized preoperatively with polyvinyl alcohol particles. Complete surgical excision was possible in each patient and the plane of resection was adventitial. In three cases, early ligation of the external carotid artery facilitated the resection. In two patients, the vagus nerve was sacrificed because of tumour involvement. No operative mortality was observed and no vascular complication occurred. In addition to the patient with preoperative neurologic symptoms, three patients developed peripheral nerve deficits (vagus and hypoglossal nerves) postoperatively. Two of these deficits were transient. These peripheral neurologic complications were observed with the largest tumour sizes. Two cases were malignant (lymph nodes and bony metastases). These two patients received postoperative radiotherapy. The mean follow-up period 63 +/- 19 months. No patient developed local recurrence during the follow-up. Two patients died during the follow-up, one for condition unrelated to their disease and the second from metastatic dissemination. In conclusion, carotid chemodectomas may be safely resected. The best way to minimize the rate of complications is to operate them at an early stage of evolution.
A series of 29 well-documented and properly analysed patients with thrombangiitis obliterans (Buerger's disease) is presented. The diagnosis of Buerger's disease was based on following criteria: smoking history, onset before the age of 50 years, infrapopliteal arterial occlusive disease, either upper limb involvement or phlebitis migrans, absence of atherosclerotic risk factors other than smoking. In the last 10 years (1986-1996), we identified 29 patients who met these rigid criteria. There were 24 men and 5 women, aged 32.4 years at the moment of the disease first clinical symptom. The cumulative tobacco use averaged 16 pack-years for each patient. The initial symptom was limited gangrene of a toe (n = 9) or a finger (n = 2), foot claudication (n = 6), calf claudication (n = 3), rest pain (n = 3), migratory superficial phlebitis (n = 4), and Raynaud phenomenon (n = 2). Angiography and/or Doppler ultrasound revealed digital, pedal and calf artery involvement in all patients, with proximal extension in ten patients (femoropopliteal in ten, including three cases with external iliac artery involvement). Seven patients had also evidence of upper limb involvement. Histologic proof was available in only seven patients. Only nine patients completely stopped smoking. Treatment was exclusively medical in five cases. Twenty-four underwent sympathectomy (20 at lumbar, and four at thoracic level), with good immediate result in 16. In 11 patients a vascular reconstruction was done (eight femorocrural and three iliofemoral bypasses), with a patency rate of only 36% at two years. Amputation was required in 16 patients (a mean of 2.7 amputations per patient) at one or more levels: toe (n = 19), forefoot (n = 5), below knee (n = 8), above knee (n = 2), finger (n = 3). Two patients ended up with bilateral leg amputation. Overall, 23% (7/30) of the patients required major leg amputation during the course of the disease. Disease progression was moderately related to continued tobacco use. Buerger's disease still entails considerable risk of major amputation. Complete abstinence from tobacco use is crucial to expect stabilization of the process. However, in advanced stages of the disease and despite cessation of smoking recurrent episodes of ischaemia or tissue loss are not excluded.