Functional outcome after antegrade femoral nailing: a comparison of trochanteric fossa versus tip of greater trochanter entry point.

OBJECTIVES: This study was performed to explore the relationship between entry point-related soft tissue damage in antegrade femoral nailing and the functional outcome in patients with a proximal third femoral shaft fracture. DESIGN: Retrospective clinical trial. SETTING: Level I university trauma center. PATIENTS: Seventeen patients with a high femoral shaft fracture treated with an antegrade femoral nail joined the study. INTERVENTION: Nine patients with an Unreamed Femoral Nail (UFN; Synthes, Bettlach, Switzerland) inserted at the trochanteric fossa and eight patients with a long Proximal Femoral Nail (PFN; Synthes) inserted at the tip of the greater trochanter. MAIN OUTCOME MEASUREMENTS: Pain, gait, nerve, and muscle function along with endurance. RESULTS: Five patients with a UFN had a positive Trendelenburg sign and a reinnervated superior gluteal nerve after initial injury of the nerve at operation. None of these findings occurred in the long PFN group (P = 0.01). Isokinetic measurements showed diminished abduction as well as external rotator function in the UFN group rather than in the long PFN group. Leg endurance was significantly lower in patients with a UFN. CONCLUSIONS: Compared with the trochanteric fossa, femoral nailing through the greater trochanter tip may decrease the risk of damage to the superior gluteal nerve and intraoperative damage to the muscular apparatus of the hip region, resulting in some improved muscle function. Therefore, a lateral entry point may be a rational alternative for conventional nailing through the trochanteric fossa.

Moxonidine normalizes sympathetic hyperactivity in patients with eprosartan-treated chronic renal failure.

Enalapril and losartan reduce but not normalize sympathetic hyperactivity in patients with hypertensive chronic renal failure (CRF). This study assessed the effect of chronic eprosartan on BP and sympathetic activity, and assessed the effect of moxonidine during chronic eprosartan treatment. In 11 stable patients with CRF (creatinine clearance 47 +/- 10 ml/min), muscle sympathetic nerve activity (MSNA; peroneal nerve), BP, and baroreceptor sensitivity were measured in the absence of antihypertensive drugs (except diuretics) during chronic eprosartan therapy (600 mg for 6 wk) and in 9 patients after moxonidine (0.2 mg for 6 wk) was added. Normovolemia was controlled by diuretics and confirmed by extracellular fluid volume measurements. BP, heart rate, and MSNA were higher in patients than in 22 controls. During eprosartan therapy, mean arterial pressure (111 +/- 9 to 98 +/- 7 mmHg, P < 0.001), heart rate (71 +/- 10 to 65 +/- 8 bpm, P < 0.001), and MSNA (35 +/- 10 to 27 +/- 8 bursts/min, P < 0.001) decreased. After the addition of moxonidine (n = 9), a further reduction of mean arterial pressure to 89 +/- 7 mmHg (P < 0.05) and of MSNA to 20 +/- 10 bursts/min (P < 0.05) occurred. Sympathetic activity in patients with CRF can be normalized, and angiotensin II-independent sympathetic hyperactivity contributes to the pathogenesis of renal hypertension. Sympathetic hyperactivity is associated with poor cardiovascular outcomes, implying that reduction might be beneficial to the patients. The addition of moxonidine to angiotensin II antagonist treatment might be appropriate.