Between October 1972 and December 1980, 139 post-traumatic brachial plexus palsies were operated upon by the same surgeon. The results of 63 are reported with a follow up of at least three years for the 32 complete palsies and two years for the 31 partial palsies. The protocol for examination and surgical repair is described. Major repairs were performed in 48, including suture, interfascicular grafting and nerve transfer. The remaining 15 had a neurolysis. The results are given for each type of lesion and for each kind of repair. Two series of complete palsies, one treated operatively, the other conservatively, are compared. It is concluded that surgical repair gives good results in partial palsies and in some complete palsies. Nerve transfer or graft gives some improvement but the usefulness of the limb remains disappointing.

Ligamentous instability of the ankle joint can be confirmed by radiographs taken in two planes. The place of the anteroposterior varus stress view is established, but the lateral view which shows anterior subluxation of the talus is frequently omitted. The anatomical significance of the two stress views has been determined by dividing different components of the lateral ligament of 20 cadaveric ankles and noting the subluxation that resulted from these procedures. A clinical assessment was then made of 54 ankles (46 patients) with radiological evidence of instability when subjected to varus and anterior stress. Anterior subluxation was found to be considerably more common than varus tilt, and it is therefore suggested that the lateral stress view should be an essential part of the investigation of the unstable ankle.

1. Experiments show relative weakness of the second metatarsal epiphysis at a certain stage of epiphysial maturation.

2. It is shown that at this stage Freiberg's infraction is likely to occur.

3. It has been demonstrated that even gross comminution with disruption of the articular cartilage of the second metatarsal head is compatible with a radiograph of almost normal appearance.

Background

Symptoms of obstetric brachial plexus injury (OBPI) vary widely over the course of time and from individual to individual and can include various degrees of denervation, muscle weakness, contractures, bone deformities and functional limitations. To date, no universally accepted overall framework is available to assess the outcome of patients with OBPI. The objective of this paper is to outline the proposed process for the development of International Classification of Functioning, Disability and Health (ICF) Core Sets for patients with an OBPI.

We investigated the effect of progesterone on the nerve during lengthening of the limb in rats. The sciatic nerves of rats were elongated by leg lengthening for ten days at 3 mm per day. On alternate days between the day after the operation and nerve dissection, the progesterone-treated group received subcutaneous injections of 1 mg progesterone in sesame oil and the control group received oil only. On the fifth, tenth and 17th day, the sciatic nerves were excised at the midpoint of the femur and the mRNA expression level of myelin protein P0 was analysed by quantitative real time polymerase chain reaction. On day 52 nodal length was examined by electron microscopy, followed by an examination of the compound muscle action potential (C-MAP) amplitude and the motor conduction velocity (MCV) of the tibial nerve on days 17 and 52. The P0 (a major myelin glycoprotein) mRNA expression level in the progesterone-treated group increased by 46.6% and 38.7% on days five and ten, respectively. On day 52, the nodal length in the progesterone-treated group was smaller than that in the control group, and the MCV of the progesterone-treated group had been restored to normal.

Progesterone might accelerate the restoration of demyelination caused by nerve elongation by activating myelin synthesis.

Perilesional changes of chronic focal osteochondral defects were assessed in the knees of 23 sheep. An osteochondral defect was created in the main load-bearing region of the medial condyle of the knees in a controlled, standardised manner. The perilesional cartilage was evaluated macroscopically and biopsies were taken at the time of production of the defect (T0), during a second operation one month later (T1), and after killing animals at three (T3; n = 8), four (T4; n = 8), and seven (T7; n = 8) months. All the samples were histologically assessed by the International Cartilage Repair Society grading system and Mankin histological scores. Biopsies were taken from human patients (n = 10) with chronic articular cartilage lesions and compared with the ovine specimens. The ovine perilesional cartilage presented with macroscopic and histological signs of degeneration. At T1 the International Cartilage Repair Society ‘Subchondral Bone’ score decreased from a mean of 3.0 (sd 0) to a mean of 1.9 (sd 0.3) and the ‘Matrix’ score from a mean of 3.0 (sd 0) to a mean of 2.5 (sd 0.5). This progressed further at T3, with the International Cartilage Repair Society ‘Surface’ grading, the ‘Matrix’ grading, ‘Cell Distribution’ and ‘Cell Viability’ grading further decreasing and the Mankin score rising from a mean of 1.3 (sd 1.4) to a mean of 5.1 (sd 1.6). Human biopsies achieved Mankin grading of a mean of 4.2 (sd 1.6) and were comparable with the ovine histology at T1 and T3.

The perilesional cartilage in the animal model became chronic at one month and its histological appearance may be considered comparable with that seen in human osteochondral defects after trauma.

Clavicular fractures are occasionally responsible for lesions of the brachial plexus. The symptoms are usually delayed and due to compression by hypertrophic callus, nonunion or a subclavian pseudoaneurysm.

We describe a patient in whom a displaced bone fragment was pressing on the retroclavicular part of the brachial plexus, leading to early symptoms of a lesion of the posterior cord. Internal fixation of the clavicle and external neurolysis of the brachial plexus gave an almost full recovery.

Darrach's procedure was performed for post-traumatic symptoms in the inferior radio-ulnar joint in 36 patients, who were reviewed after a mean follow-up of 6 years. Only 18 of the patients had a satisfactory clinical result. Poor outcome was associated with osteoarthritis of the wrist, the occurrence of algodystrophy and a short ulnar remnant.

Surgeons are at risk from both hepatitis B and human immunodeficiency viruses. While vaccines have been developed against the former, barrier methods remain the mainstay of protection. Puncture wounds of the hand are a potential source of contamination; the protection afforded by surgical gloves has been investigated. Gloves from 280 orthopaedic operations for trauma were tested for perforations; one or more was found after 30% of the operations in gloves worn by the surgeon or scrub nurse. About 60% of the perforations were noticed at the time of penetration and most affected the dominant thumb and index finger. Puncture was more common during operations lasting more than one hour. The incidence of perforation was 19% for the outer of double gloves, 14% for a single glove and 6% for the inner of double gloves. These results indicate that surgical gloves function poorly as a protective barrier, especially in difficult, lengthy, fracture surgery. The practice of double-gloving confers increased but not absolute protection.

1. The electric potentials in undeformed rabbit tibiae were measured in vivo and in vitro.

2. Surgically traumatised soft-tissues, particularly muscle, constituted the major source of voltage in vivo (up to 22 millivolts).

3. Electrical insulation of the tibia from attached soft parts abolished the high potentials on the bone.

4. Similarly high voltages could be reproduced in an excised tibia by substituting a battery for the injured muscle.

5. Changes in voltage also could be induced by altering blood flow rates or by rapid infusion of saline into the medullary space.

6. Death of the cellular elements in bone did not alter the voltage significantly.

7. The electrical contributions of the nervous system, and of dipole components of the extracellular matrix (such as collagen), either were inconsequential or of such low magnitude as to be "masked" by the larger "injury" voltages. Supported by grants from the United States Public Health Service (AM-07822) and the National Institute of Arthritis and Metabolic Diseases (TIAM-05408).

This chamber is designed for use with conscious or unconscious patients requiring treatment with oxygen under high pressure. It can be pressurised to a maximum of 45 pounds per square inch above ambient (60 pounds per square inch absolute).

The unit consists of two parts, the pressure chamber and the control console, connected together by flexible hose. The chamber can be operated up to a distance of 100 feet from the control console and both parts are mobile.

The chamber consists of two concentrically mounted transparent cylinders, closed at the ends by domed metal caps. One end cap is detachable and can be removed, complete with the bed. The bed will accommodate a patient 6 feet 6 inches tall. The fully transparent chamber allows a complete view of the patient during treatment.

A communication system is provided between the patient and operators. A loud speaker and microphone are built into the door of the chamber and two external pick-up points are situated on the console and the fixed end cap of the chamber. Two-way or three-way conversation is possible and the patient can be temporarily isolated from the system if required.

Oxygen and electrical services must be coupled to the console. The chamber will operate directly from oxygen cylinders charged to a maximum of 1,800 pounds per square inch or from any piped supply with a minimum pressure of 75 pounds per square inch absolute.

A self-contained 12-volt direct current battery supplies the necessary electrical power. A charging unit is incorporated in the control console and this is normally connected to an alternating current supply to keep the battery fully charged. If initially the battery is fully charged the unit can be operated in a continuous pressurisation-depressurisation cycle for at least twenty-four hours without further charging.

Pressurisation and depressurisation are achieved by means of a motorised valve on the outlet of the pressure chamber. During pressurisation a variable speed motor applies a gradually increasing load to a helical spring. This in turn loads the outlet valve. By this means smooth pressure changes are obtained and the motor speed can be used to control the rate of pressure change.

Operating the pressure chamber is simple. After the patient has been placed in the chamber and the door sealed by screw-down knobs, pressurisation is started by turning a selector switch on the control console. The required working pressure can be preset or the pressure can be held at any point between ambient and the top working pressure of 45 pounds per square inch above ambient. Pressurisation stops automatically when the preset level is reached or at 45 pounds per square inch. The rate of pressurisation is selected on the console and can be varied up to a maximum of approximately 8 pounds per square inch per minute. In the same manner, depressurisation can be controlled at any rate up to 8 pounds per square inch per minute down to ambient pressure, or held at any intermediate pressure according to the wishes of the operator.

Coloured lights on the control panel indicate whether the chamber is ready for use, in the pressurisation or depressurisation state, holding a steady pressure or holding at the chosen maximum pressure.

This pressure chamber is run as an open circuit. A continuous ventilating flow of oxygen passes through the chamber to wash out carbon dioxide and water vapour.

In the event of an emergency affecting the patient, fast depressurisation controls are provided on both the chamber and the console. An electrically operated dumping valve can be triggered from the control console or the same valve operated manually from the end of the chamber. A pressure drop of one pound per square inch per second is obtained when this valve is used, and it is possible to reduce from maximum pressure and remove the patient from the chamber in approximately one minute. If a total power failure should occur, a manually operated, slow depressurisation valve can be opened on the control console.

A number of sealed electrical plugs are provided in the door of the chamber. With suitable apparatus these allow electro-physiological monitoring of the patient throughout the course of the treatment.

1. A small mobile oxygen chamber is described which overcomes some of the disadvantages of using high pressure oxygen therapy in cases of general or local anoxia.

2. A case of limb ischaemia following an open fracture of the tibia and fibula is described in which such a method of treatment was used.