Bilateral Lower-Extremity Edema Caused by Iliopsoas Bursal Distention after Hip Arthroplasty.

Lower-extremity edema is encountered by internists, nephrologists, vascular specialists, and many others. We report a case of an elderly woman who presented with a painful, swollen left leg. Without a clear diagnosis, she had been taking diuretics for the past 8 years for swelling in both legs. After extensive investigation, we found that her lower-extremity edema was due to bilateral iliopsoas bursal distention secondary to degeneration of her hip prostheses. Chronic breakdown of the polyethylene component of the hip prostheses had led to a communication between the artificial joints and the iliopsoas bursae. With the aid of ultrasonographic guidance, she underwent drainage, followed by clinical and radiographic improvement. Although case reports have described leg swelling arising from extravascular compression by enlarged iliopsoas bursae, we think that this is the first case of clinically significant bilateral lower-extremity edema arising from that cause. More important than the novelty is the inappropriate use of diuretics to treat lower-extremity edema without first establishing a diagnosis.

An Emerging Role for Understanding Orthostatic Hyp'er'tension in the Cardiorenal Syndrome.

Orthostatic hypertension (OHT) is a clinically important problem increasingly recognized in persons with borderline hypertension, diabetes mellitus, and autonomic neuropathies, and in the elderly. Moreover, the association of OHT with progression of target end-organ damage, especially coronary heart disease and chronic kidney disease (CKD), and the attendant increased cardiovascular disease (CVD) and CKD risk, is gaining attention but is still underappreciated. There are various mechanisms that contribute to the development of OHT: excessive vascular adrenergic sensitivity, baroreceptor reflex abnormalities, and inappropriate activation of the renin-angiotensin-aldosterone system, which are also mechanisms that lead to cardiorenal metabolic disease (CRS). While the evidence is compelling for the clinical importance of OHT, more investigation is needed to evaluate the effects of OHT on CKD and CVD. The notion that the development of OHT is a risk factor for the development of CRS raises the need for further clinical and investigational attention to this clinical dilemma.

Ankle exercise and venous blood velocity.

Ankle exercise increases venous blood velocity while supine, but the effect of ankle exercise on venous blood velocity while sitting is not known. In this investigation, we test the hypothesis that venous blood velocity can be increased while sitting by repetitive dorsiflexion of the foot. Time-averaged peak velocity (TAPV) in the popliteal vein of 20 healthy male volunteers was measured by pulsed Doppler ultrasound at rest and during ankle exercise in the supine and sitting positions. Right popliteal vein TAPV while supine at rest was 11 cm/second (sec) (95% confidence interval [CI] =9-13 cm/sec) and with ankle exercise it increased to 24 cm/sec (95% CI =20-28 cm/sec) (p<0.0001). With sitting at rest, right popliteal vein blood TAPV decreased from 11 cm/sec to 3 cm/sec (95% CI = 2-4 cm/sec) (p<0.0001). With ankle exercise while sitting, right popliteal vein TAPV increased to 18 cm/sec (95% CI =15-21 cm/sec) (p<0.0001). In conclusion, in both the supine and sitting positions, ankle exercise increased venous blood velocity, thereby transiently reducing a tendency toward venous stasis. Such ankle exercise might be useful in the prevention of stasis-induced deep venous thrombosis.