Alvimopan, a peripherally acting mu-opioid receptor antagonist, compared with placebo in postoperative ileus after major abdominal surgery: results of a randomized, double-blind, controlled study.

BACKGROUND: Alvimopan is a peripherally acting mu-opioid receptor (PAM-OR) antagonist for accelerating gastrointestinal recovery after surgery. METHODS: Patients undergoing open laparotomy (bowel resection, n = 418; hysterectomy, n = 197) were randomized to receive alvimopan 6 or 12 mg or placebo orally > or = 2 h before surgery and then b.i.d. until hospital discharge (up to 7 days). The primary efficacy endpoint was time to gastrointestinal (GI) recovery (measured by toleration of solid food and passage of flatus/stool; GI-3). Secondary endpoints included time to GI-2 recovery (toleration of solid food and passage of stool) and hospital discharge order written (DCO). RESULTS: Alvimopan did not significantly accelerate GI-3 compared with placebo [6 mg: hazard ratio (HR) = 1.20, p = 0.080; 12 mg: HR = 1.24, p = 0.038). However, after adjustment for significant covariates (sex/surgical duration), benefits were significant for both doses (6 mg: HR = 1.24, p = 0.037; 12 mg: HR = 1.26, p = 0.028). Alvimopan also significantly accelerated time to GI-2 (6 mg: HR = 1.37, p = 0.008; 12 mg: HR = 1.33, p = 0.018) and DCO (6 mg: HR = 1.31, p = 0.008; 12 mg: HR = 1.28, p = 0.015). Adverse events were similar between groups. CONCLUSIONS: Alvimopan (6 or 12 mg) accelerates GI recovery and is well tolerated in patients undergoing open laparotomy.

Quantitative measurement of ankle passive flexibility using an arthrometer on sprained ankles.

OBJECTIVE: The purpose of this study was to quantitatively examine the flexibility of sprained ankles using an arthrometer device and compare the differences in flexibility between ankles following the first sprains and ankles with repeated severe sprains and chronic symptoms. DESIGN: A retrospective in vivo study was used. BACKGROUND: Many in vitro studies have demonstrated a significant role of joint flexibility in determining mechanical laxity of human cadaveric ankles after sectioning of the lateral ligaments, but few in vivo studies have used the technique to provide objective measurement on the sprained ankles. Furthermore, there is a lack of extensive studies that compared the difference in the ankle flexibility between ankles following the first sprain and ankles with multiple repeated severe sprains and chronic symptoms. METHODS: A total of 27 subjects with unilateral ankle sprains participated in this study. The subjects were divided into a first injury group (group A, n=12) and a chronic symptom group (group B, n=15) based on the history of their ankle injuries. The ankle flexibility in anterior drawer and inversion/eversion tests was measured in both ankles of the subjects using an arthrometer device, the ankle flexibility tester -- a six-degree-of-freedom instrumented linkage used for measurements of applied forces/moments and resultant rotations and/or translations of the ankle joint complex. The difference in ankle flexibility between the injured ankle and the contralateral intact side was analyzed. RESULTS: The flexibility in anterior drawer test of the injured ankles significantly increased compared to the intact ankles of the same individual in group B, but the same difference was not significant in group A. There were more subjects in group B (46.6%) than in group A (33.3%) who showed a sign of mechanical laxity in their injured ankles. CONCLUSIONS: The results indicated that the approach with measurement of ankle flexibility may be a potential tool used to detect the mechanical laxity in the sprained ankles. A tendency was found that patients with multiple ankle sprains and chronic symptoms had a higher occurrence rate of mechanical laxity. The result of the present study may also be interpreted that the ankles with mechanical laxity had higher risk of re-injury and leading to chronic symptoms.

Changes in the flexibility characteristics of the ankle complex due to damage to the lateral collateral ligaments: an in vitro and in vivo study.

This study was part of a long-term effort to develop a reliable diagnostic procedure for ankle ligament injuries. Earlier efforts led to the development and validation of a six-degrees-of-freedom instrumented linkage capable of measuring the flexibility characteristics of the ankle complex in vitro and in vivo. The major goal of the present study was to determine if these flexibility measurements are sufficiently sensitive to detect the presence of damage to the lateral collateral ligaments of the ankle joint both in vitro and in vivo. The in vitro testing was conducted on the legs from six fresh cadavers before and after serial sectioning of the anterior talofibular ligament and the calcaneofibular ligament. The flexibility in inversion-eversion, anterior drawer, and internal-external rotation was measured before and after resection of the ligaments. The in vivo testing was conducted on five patients with unilateral injuries to the ankle ligament. The flexibility evaluation used for in vitro specimens was also performed on both the injured and the intact ankles. For the in vitro testing, the data analysis was based on comparison of flexibility values before and after resection of the ligaments, whereas the data analysis for the in vivo testing was based on comparison of the flexibility of the injured joint with that of the intact contralateral joint. The results of the in vitro study indicated that both an isolated rupture of the anterior talofibular ligament and combined damage of the anterior talofibular and calcaneofibular ligaments produce statistically significant changes in flexibility. Furthermore, the most sensitive parameters to the presence of ligament injuries were found to be early flexibility in anterior drawer, early flexibility in inversion, and the amount of coupling between internal rotation and inversion. These parameters provided a basis for differentiating between an isolated injury to the anterior talofibular ligament and a combined anterior talofibular and calcaneofibular ligament injury. For an isolated anterior talofibular ligament injury, a significant increase in flexibility in anterior drawer was present, whereas the increase in inversion flexibility or in the amount of coupling was insignificant. However, the increases in inversion flexibility and the amount of coupling became significant when both ligaments were involved. The results of the in vivo study indicated that significant changes in flexibility can be detected in patients with lateral ankle injuries. Finally, both the in vitro and in vivo results suggest that development of a reliable diagnostic test for ankle ligament injury based on changes in passive flexibility may be possible.

Peroneal tubercle osteochondroma.

Osteochondromas are common bone lesions; however, their occurrence in the calcaneus is rare. A discussion of this lesion along with an unusual case and related findings are presented.

Acro-osteolysis.

Acro-osteolysis is a common radiographic finding in the upper or lower extremity. It may be idiopathic, part of a primary osteolysis syndrome, associated with a systemic disorder, traumatically induced, or caused by environmental toxins. Recognition of this process and its associated disorders is essential for complete patient care. This paper discusses the definition, etiologies, pathogenesis, and radiographic findings of acro-osteolysis.

A double-blind crossover study comparing two doses of Duranest (etidocaine) 1% with a fixed dose of Sensorcaine (bupivacaine) 0.5% utilizing infiltration regional blocks of the fifth ray.

Two local anesthetics, Duranest 1% (etidocaine HCl) and Sensorcaine 0.5% (bupivacaine HCl), were tested against each other in dose-related blocks of the fifth ray. This study was conducted under double-blind cross-over conditions using 24 healthy volunteers. It was found that 4 ml. of either agent was sufficient to anesthetize the fifth ray area in all but 4.2% of the injections and 8 ml. of etidocaine always accomplished complete fifth ray anesthesia. Also, 4 ml. of etidocaine was found to have a more rapid onset and longer duration than the same volume of bupivacaine, 6.3 vs. 8.3 min. onset, and 487 vs. 449 min. duration, respectively. Pain and burning upon injection of either bupivacaine or etidocaine was encountered in 70% of the subjects tested. Residual pain was noted in some of the subjects given etidocaine after complete resolution of sensory anesthesia. Residual pain was not noted in any of the subjects given bupivacaine. Etidocaine was found to have a more rapid onset and a longer duration than bupivacaine or a lidocaine-bupivacaine mixture, and was thus found to be a superior agent in the subjects tested.

Attack of sea urchin eggs by dogfish phagocytes: model of phagocyte-mediated cellular cytotoxicity.

To test whether lysosomal degranulation of phagocytes is associated with antibody-dependent cytotoxicity, eggs of Arbacia punctulata were used as targets for blood phagocytes of Mustelus canis. Eggs were coated with heat-aggregated dogfish IgM and exposed to phagocytes, and cytolysis of eggs was observed by Nomarski optics. Phagocytes adhered, degranulated, and raised fertilization membranes resembling those induced by sperm or ionophore A23187. Lysis was then observed as damage radiating from the point of phagocyte-egg contact. By 4 hr, coated eggs exposed to phagocytes released 8.9, 12.3, and 7.4% of total catalase (EC 1.11.1.6), beta-glucuronidase (EC 3.2.1.31), and superoxide dismutase (EC 1.15.1.1) into the medium. Cytotoxic enzyme release significantly exceeded that from uncoated eggs incubated with phagocytes or eggs alone (uncoated or coated). Because activated eggs release a neutral protease, it was considered possible that this enzyme might be responsible for autolysis of eggs. This possibility was excluded because (i) lysis of eggs was not inhibited by soybean trypsin inhibitor (SBTI) whereas the egg protease was sensitive to SBTI, and (ii) the major trypsin-like activity of phagocytes was not inhibited by SBTI. These experiments demonstrate that Ig-coated cells are first activated, and then killed, when exposed to degranulating phagocytes and suggest that enzymes from attacking phagocytes, and not target cells, are responsible for cell death.