Iliac Crest Herniation Secondary to Autogenous Bone Grafting Found on Osteopathic Examination.

Surgical repair of difficult or nonunion fractures is frequently performed with autogenous bone grafts, most commonly from the iliac crest. Complications from this procedure may include vessel injury, nerve injury, pelvic instability, bowel herniation, and ileus. The authors report a case of iliac crest herniation in a patient presenting with a small-bowel obstruction 2 years after anterior iliac crest graft harvest for an open reduction and internal fixation repair of a right humeral shaft fracture. An emergency operation revealed that the right colon had herniated through an opening in the right iliac crest. The appendix had adhered to new osseous bone formed postoperatively, requiring an appendectomy. The hernia defect was successfully repaired with polypropylene mesh. A high index of suspicion for graft site herniation is needed for patients with a history of iliac crest bone grafting who present with symptoms of abdominal pain, flank or hip pain, ileus, or small-bowel obstruction.

A role for corticotropin releasing factor (CRF) in ethanol consumption, sensitivity, and reward as revealed by CRF-deficient mice.

RATIONALE: Corticotropin-releasing factor (CRF) plays an integral role in mediating stress responses and anxiety. However, little is known regarding the role of CRF in ethanol consumption, a behavior often associated with stress and anxiety in humans. OBJECTIVE: The present study sought to determine the role of CRF in ethanol consumption, locomotor sensitivity and reward by examining these behaviors in C57BL/6J x 129S mice with a targeted disruption in the gene encoding the CRF prohormone. METHODS: Male wild-type and CRF-deficient mice were given concurrent access to ethanol and water in both limited and unlimited-access two-bottle choice paradigms. Taste reactivity (saccharin or quinine vs water) was examined in a similar manner under continuous-access conditions. Blood ethanol levels and clearance were measured following limited ethanol access as well as a 4-g/kg i.p. injection of ethanol. Locomotor stimulant effects of ethanol were measured in an open-field testing chamber, and the rewarding effects of ethanol were examined using the conditioned place preference paradigm. RESULTS: CRF-deficient mice displayed normal body weight, total fluid intake, taste reactivity and blood ethanol clearance, but consumed approximately twice as much ethanol as wild types in both continuous- and limited-access paradigms. CRF-deficient mice failed to demonstrate a locomotor stimulant effect following acute administration of ethanol (2 g/kg i.p.), and also failed to demonstrate a conditioned place preference to ethanol at 2 g/kg i.p., but did display such a preference at 3 g/kg i.p. CONCLUSIONS: CRF deficiency may lead to excessive ethanol consumption by reducing sensitivity to the locomotor stimulant and rewarding effects of ethanol.

Effects of acute acamprosate and homotaurine on ethanol intake and ethanol-stimulated mesolimbic dopamine release.

The purpose of the present study was to determine the acute effects of the anticraving compound acamprosate (calcium acetylhomotaurinate) and the closely related compound homotaurine on ethanol intake and ethanol-stimulated dopamine release in the nucleus accumbens. Male rats were treated with acamprosate (200 or 400 mg/kg intraperitoneally, i.p.) or homotaurine (10, 50, or 100 mg/kg i.p.) 15 min prior to access to 10% ethanol and water for 1 h in a two-bottle choice restricted access paradigm. A separate group of rats was implanted with microdialysis probes in the nucleus accumbens and given an acute injection of ethanol (1.5 g/kg i.p.) that was preceded by saline, acamprosate, or homotaurine. Acamprosate and homotaurine dose-dependently reduced ethanol intake and preference. These compounds also delayed or suppressed ethanol-stimulated increases in nucleus accumbens dopamine release, suggesting that acamprosate and homotaurine may reduce ethanol intake by interfering with the ability of ethanol to activate the mesolimbic dopamine reward system.