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A probable cause of popliteal artery entrapment is proposed. The medial head of the gastrocnemius muscle during its embryological development crosses the popliteal fossa from lateral to medial. It is proposed that the migrating medial head carries the popliteal artery and vein across the fossa and entraps them against the medial condyle of the femur. Dissection of 86 anatomical specimens revealed two cases of unilateral and one case of bilateral entrapment of both popliteal vessels. Two surgical cases of popliteal entrapment are presented. This entrapment syndrome is a remedial cause of claudication and when considered, it is readily diagnosed and surgical correction is effective. Because of distal embolisation and occlusions, early recognition and treatment is desirable. Forty-seven cases from the literature are reviewed as to the entrapment type and the age and sex of the patients.

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Oral controlled-release oxycodone was twice as potent as oral controlled-release morphine in this single-dose, relative potency assay. When converting patients from oral morphine to oral oxycodone, an initial oral oxycodone dose of one-half the oral morphine dose is recommended.

We present a consecutive series of nine patients who were referred to us because of arthrofibrosis (loss of > 15 degrees of extension) after intraarticular anterior cruciate ligament reconstruction using autogenous patellar tendon (eight patients) or semitendinosus (one patient) graft. Eight patients had surgery within 2 weeks of injury. All patients had been immobilized in flexion after the anterior cruciate ligament reconstruction and they had failed to improve despite vigorous physical therapy and other closed methods of treatment. The mean time from anterior cruciate ligament reconstruction to the subsequent surgery was 10.2 months (range, 3 to 14). The patients underwent an outpatient arthroscopic anterior scar resection, notchplasty, a closed knee manipulation for flexion, and extension casting. Serial daily extension cast changes allowed the patients to obtain full extension, which was maintained by a bivalved extension splint for bedtime use. Flexion was actively sought by aggressive outpatient physical therapy. All patients except one noted near-normal ultimate range of motion. One patient could only attain 10 degrees short of flat extension at the end of his rehabilitation and was considered a failed result. At final followup (mean, 31 months), no patient complained of symptoms of instability, all had a normal gait, and all but one were able to return to athletic activities.

SummaryWe report 13 cases of presumed rocuronium-induced anaphylaxis in which sugammadex was administered with the intention of reversing the immunological reaction. Of these 13 cases, eight (62%) were later confirmed to be type-1 hypersensitivity reactions to rocuronium, three (23%) were triggered by an antibiotic and two (15%) were non-immunologically mediated. Response to treatment was scored by the treating anaesthetist, and compared with haemodynamic and inotrope measurements from the resuscitation and anaesthetic records. Haemodynamic improvement was seen in only six (46%) cases, three of which were associated with a non-rocuronium trigger. Of the three cases in which the treating anaesthetist thought that sugammadex had been beneficial, one was not caused by rocuronium, one had no improvement in blood pressure and one required 8.5 times as much adrenaline in boluses after, compared with the period before, sugammadex administration. These data suggest that sugammadex does not modify the clinical course of a suspected hypersensitivity reaction.