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Between 2005 and 2010 ten consecutive children with high-energy open diaphyseal tibial fractures were treated by early reduction and application of a programmable circular external fixator. They were all male with a mean age of 11.5 years (5.2 to 15.4), and they were followed for a mean of 34.5 months (6 to 77). Full weight-bearing was allowed immediately post-operatively. The mean time from application to removal of the frame was 16 weeks (12 to 21). The mean deformity following removal of the frame was 0.15° (0° to 1.5°) of coronal angulation, 0.2° (0° to 2°) sagittal angulation, 1.1 mm (0 to 10) coronal translation, and 0.5 mm (0 to 2) sagittal translation. All patients achieved consolidated bony union and satisfactory wound healing. There were no cases of delayed or nonunion, compartment syndrome or neurovascular injury. Four patients had a mild superficial pin site infection; all settled with a single course of oral antibiotics. No patient had a deep infection or re-fracture following removal of the frame. The time to union was comparable with, or better than, other published methods of stabilisation for these injuries. The stable fixator configuration not only facilitates management of the accompanying soft-tissue injury but enables anatomical post-injury alignment, which is important in view of the limited remodelling potential of the tibia in children aged > ten years. Where appropriate expertise exists, we recommend this technique for the management of high-energy open tibial fractures in children.

A 31-year-old man from mainland China presented with sudden onset weakness of limbs of eight hours duration. He had woken up from bed with weakness. He was not on any medication; both parents and brother are healthy. On examination he had motor weakness with diminished deep jerks. Non-tender hepatomegaly was present.Investigations revealed normal blood counts, urea, creatinine, glucose and electrolytes were normal, creatine kinase 1105 U/1 (reference range: 10-195), alanine transaminase 68 U/l (5-40), aspartate transaminase 49 U/1 (6-37), alkaline phosphatase 180 U/1 (98-279), glutamyl transferase 128 U/I (10-50), plasma viscosity 1.57 mPas at 250C (1.50-1.72). Electrocardiograms were normal and chest X-ray was clear. Peak flow was 560 /min.He recovered naturally and, while awaiting other results, was discharged. He was re-admitted within a week with hypokalemia of 1.8 mmol/l (3.5 -5.5). The outstanding investigations were by then available. Free thyroxine 65.6 pmol/l (9-24), thyroid-stimulating hormone (TSH) <0.05 mU/l (0.49-4.67), free tri-iodothyronine 24 pmol/l (4-8.3). Antiparietal cell antibodies were positive, thyroid autoantibodies were not detected, ds-DNA, antinuclear antibodies, antismooth muscle, mitochondrial and extractable nuclear antigen, and Jol were negative. Muscle biopsy did not show significant abnormalities. Electromyography and nerve conduction studies were normal. By this time creatine kinase levels had normalised. Hepatitis B surface antigen and anti-Hb E were positive and Hb E antigen was negative.

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