Synovial cyst formation complicating total hip arthroplasty: a case report.

The most frequent causes of unilateral limb swelling unrelated to trauma or surgery are deep venous thrombosis, chronic venous insufficiency, and primary lymphedema. Other important but less frequent causes include infection and neoplasm. Neoplasms may cause limb swelling, either by soft tissue enlargement or incidental compression of venous or lymphatic structures. Reported here is an unusual case of a patient with unilateral leg swelling and an inguinal mass presenting years after total hip arthroplasty. The unilateral leg swelling was caused by compression of the right common femoral vein by a synovial cyst arising from the hip joint. Although only 2 cases have been described in the literature, such cyst formation is not uncommon with loose acetabular components. The most apparent cause of cyst formation was polyethylene debris. Treatment efforts should be directed at the source of the debris intraarticularly.

Current management of coexistent intra-abdominal pathology in patients with abdominal aortic aneurysms.

In conclusion, it can be seen that coexistent intra-abdominal pathology and aortic aneurysms demands an individualized approach to determine a treatment plan for a given patient. Life expectancy must be balanced against the risk of a complication developing in either the treated or untreated condition as well as the potential for increased morbidity associated with combined procedures. If combined procedures are performed, they must be undertaken only if the aneurysm resection has gone smoothly. Efforts must be directed at protecting the prosthetic graft from direct contamination that may accompany the secondary procedure. In general, the symptomatic lesion should be treated first. If both conditions are asymptomatic, the relative risks and benefits of treatment must be balanced against the probability that one or both of the conditions will become symptomatic.

Perimalleolar subcutaneous tissue pressure effects of elastic compression stockings.

PURPOSE: We hypothesized that the clinical benefit of elastic compression stockings (ECS) is at least in part due to an increase in subcutaneous pressure that may promote resorption of extracellular fluids, providing more efficient diffusion of oxygen and nutrients from the microcirculation to the skin and subcutaneous tissues. METHODS: To test this hypothesis we designed and standardized a device for measuring subcutaneous pressure in patients. We then measured the supine perimalleolar subcutaneous pressure from a single limb in four groups: group 1 consisted of control subjects (n = 8); group 2 consisted of patients with varicose veins and superficial venous insufficiency without lipodermatosclerosis or edema (n = 5); group 3 consisted of patients with deep venous insufficiency and lipodermatosclerosis but without edema (n = 8); and group 4 consisted of patients with deep venous insufficiency, lipodermatosclerosis, and clinically evident edema (n = 8). Measurements were made at baseline and after application of 20 to 30 mm Hg and 30 to 40 mm Hg ECS. RESULTS: There was no significant difference in the baseline subcutaneous pressure between the three groups without clinical edema (p > 0.05). Baseline perimalleolar pressure was elevated, however, in group 4 patients compared with groups 1, 2, and 3 (p < 0.05). All three groups with chronic venous insufficiency (CVI) (groups 2, 3, 4) demonstrated increases in subcutaneous pressure with application of ECS, which was statistically significant in groups 3 and 4. There was no difference between the increase in perimalleolar subcutaneous pressure induced by 20 to 30 mm Hg or 30 to 40 mm Hg ECS in groups 3 and 4. CONCLUSIONS: Patients with CVI and edema have significant elevations in supine resting perimalleolar subcutaneous pressure compared with control subjects and patients with CVI without edema. Twenty to 30 mm Hg and 30 to 40 mm Hg ECS increased measured perimalleolar subcutaneous pressure in patients with CVI with and without clinical edema but not in control patients. These results suggest the mechanism of benefit of ECS in patients with CVI is due at least in part to an increase in subcutaneous pressure that may act to promote more efficient absorption of perimalleolar extracellular fluid.

The association of elevated plasma homocyst(e)ine with progression of symptomatic peripheral arterial disease.

Plasma homocyst(e)ine (the sum of free and bound homocysteine, homocystine, and the mixed disulfide homocysteine-cysteine, expressed as homocysteine) levels were determined by high performance liquid chromatography in 214 patients with symptomatic (claudication, rest pain, gangrene, amputation) lower extremity arterial occlusive disease and/or symptomatic (stroke, cerebral transient ischemic attacks) cerebral vascular disease and in 103 control persons. Mean plasma homocyst(e)ine was significantly higher in patients than in controls (14.37 +/- 6.89 nmol/ml vs 10.10 +/- 2.16, p less than 0.05). Thirty-nine percent of patients (83 of 214) had plasma homocyst(e)ine values greater than control mean + 2 standard deviations. Plasma homocyst(e)ine values were contrasted to age, male sex, diabetes, hypertension, smoking, renal failure, and plasma cholesterol. No difference was found in the incidence and/or level of any of these risk factors when patients with normal plasma homocyst(e)ine were compared to those with elevated plasma homocyst(e)ine, both by univariate and multivariate analysis. Patients with elevated plasma homocyst(e)ine were more likely to demonstrate clinical progression of lower extremity disease and of coronary artery disease, but not of cerebral vascular disease than were patients with normal plasma homocyst(e)ine, and the rate of progression was more rapid (p = 0.002). Progression of lower extremity disease as assessed in the vascular laboratory was also more common in patients with elevated plasma homocyst(e)ine (p = 0.01). We conclude that elevated plasma homocyst(e)ine is an independent risk factor for symptomatic lower extremity disease or cerebral vascular disease or both. Symptomatic patients with lower extremity disease and with elevated plasma homocyst(e)ine also appear to have more rapid progression of disease.

The influence of elastic compression stockings on deep venous hemodynamics.

To determine the effect of elastic compression stockings on deep venous hemodynamics we measured ambulatory venous pressure, venous refill time, maximum venous pressure with exercise, amplitude of venous pressure excursion, and duplex-derived common femoral and popliteal vein diameter and peak flow velocities with and without stockings in 10 healthy subjects and 16 patients with chronic deep venous insufficiency. The effects of below-knee and above-knee 30 to 40 torr and 40 to 50 torr gradient stockings were studied. Despite documentation of substantial stocking compressive effects by skin pressure measurements, neither below-knee or above-knee elastic compression stockings significantly improved ambulatory venous pressure, venous refill time, maximum venous pressure with exercise, or the amplitude of venous pressure excursion in healthy patients or in patients with deep venous insufficiency (p greater than 0.05). In patients with deep venous insufficiency stockings modestly increased popliteal vein diameter and flow velocity in the upright resting position (p less than 0.02). After tiptoe exercise without stockings deep venous peak flow velocity increased in healthy patients and in patients with deep venous insufficiency by a mean of 103% in the popliteal vein and 46% in the common femoral vein (p less than 0.01). With the application of elastic compression stockings only modest augmentation of deep venous flow velocity occurred in both groups above that seen in the bare leg after exercise. Thus elastic compression stockings did not improve deep venous hemodynamic measurements in patients with deep venous insufficiency. The beneficial effects of stockings in the treatment of deep venous insufficiency must relate to effects other than changes in deep venous hemodynamics.