Background: Acute pain leads to adverse physiological and psychological disturbances. Hence, this study was done to evaluate and compare the onset and duration of sensory anesthesia, motor paralysis and duration of analgesia using 0.5% plain bupivacaine, with clonidine (2μg/kg) in patients posted for lower abdominal and lower limb surgeries under epidural anaesthesia. Materials and methods: 62 Patients posted for elective lower abdominal, gynaecological and lower limb surgeries under epidural anesthesia, aged 18 to 60 years, height more than 150 cms of ASA physical status 1 or 2 were included. All patients were randomized into two groups of 31 individuals each. Results: Clonidine in the dose of 2μg/kg added to bupivacaine injected into epidural space significantly prolonged the duration of analgesia when compared to bupivacaine alone. No effect on the onset of sensory and motor blockade was observed. However, it increases the duration of motor blockade. Clonidine also has effect on sedation level, pulse rate and mean arterial blood pressure. Conclusion: Clonidine causes increased sedation; fall in pulse rate and mean arterial blood pressure, which however, did not require active intervention in this study.

Background:Brown syndrome is a rare ocular motility disorder which has been reported in JRA, RA and SLE but never in a patient with scleromyositis.Objectives:To report the first case of Brown syndrome in a patient with scleromyositis and increase awareness of this condition.Methods:A case report and discussion.Results:The patient was diagnosed with scleromyositis, at the age of 34, after presenting with arthralgia, sclerodactyly, skin pigmentation, Raynaud’s phenomenon, mild muscle weakness and dyspnoea. His labs were CRP 47 mg/L, CK 868 IU/L, ANA strongly positive; anticentromere Ab negative and Anti-PM/Scl-75 and Anti- PM/Scl-100 Ab positive. HRCT chest showed extensive pulmonary fibrosis with lower lobe honeycombing. TLCO was 3.98 (33% of predicted).He was initially managed with high dose steroids and pulsed IV cyclophosphamide with azathioprine for maintenance therapy. His lung disease stabilised and myositis resolved but he continued to develop calcinosis cutis so was switched to 6 monthly IV rituximab.6 years later, he developed morning headaches with intermittent diplopia, described as double vision in vertical gaze with one image being above the other. Episodes lasting 10 minutes to 2 hours. Examination showed normal visual acuity and fundoscopy, no peripheral or eye muscle weakness.Investigations to exclude myasthenia gravis, cerebral vasculitis and atypical infection were organised (MRI, AChR antibody, lumbar puncture, MRA) and were normal.Because of intermittent nature of his episodes, his eye examination was always normal but he captured images in disconjugate gaze with right eye looking upwards and outwards when trying to look straight (Figure 1). Occasionally this was associated with orbital pain and an audible click. These features are suggestive of Brown syndrome.He continues to have recurrent episodes despite immunosuppression but prednisolone 20mg daily for 1-2 days at onset of each attack causes rapid resolution of symptoms.Figure 1.Right eye looking upwards and outwards when trying to look straightConclusion:Scleromyositis is an overlap syndrome of scleroderma and dermatomyositis. Muscle involvement is mild and clinical presentation can be variable. The PM/Scl antibodies are highly characteristic of the syndrome. (1)Brown syndrome is an ocular motility disorder, first described in 1950, characterized by the inability to fully elevate the affected eye in adduction due to pathology of the superior oblique tendon sheath. (2)It can be congenital or acquired, viz, trauma, surgery or sinusitis and also been described in RA, JIA and SLE. (3)If superior oblique tendon cannot relax or slide freely through the trochlea then the affected eye cannot depress completely, leading to diplopia on upward gaze. (4) In inflammatory disease it is thought that swelling of the posterior part of the superior oblique tendon or tenosynovitis are likely causes of the tendon sheath abnormality. (4) This is likely to be the case in this patient because his symptoms are recurrent, respond to steroids and tend to occur more towards the end of rituximab cycles.Recognition of this syndrome is important because invasive investigations can be avoided. Also, intermittent diplopia in a patient with autoimmune disease is suggestive of myasthenia gravis which maybe incorrectly diagnosed.Finally, this case demonstrates the syndrome can be easily managed with short courses of oral steroids, although patients who are already on immunosuppressant treatment may need this in addition.References:[1]Török L, Dankó K, Cserni G, Szûcs G. PM-SCL autoantibody positive scleroderma with polymyositis (mechanic’s hand: clinical aid in the diagnosis). JEADV 2004; 18: 356–359[2]Brown H W. Congenital structural muscle anomalies. In:Alien J H, ed. Strabismus ophthalmic symposium I. St Louis:CV Mosby, 1950: 205-6.[3]Cooper C, Kirwan JR, McGill NW, Dieppe PA. Brown’s syndrome: an unusual ocular complication of rheumatoid arthritis. Ann Rheum Dis 1990; 49:188-9.[4]Sandford-Smith JH. Superior oblique tendon syndrome and its relationship to stenosing tenosynovitis. Br JOphthalmol 1973; 57:859-65.Disclosure of Interests:None declared

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Case report - Introduction Chikungunya is a tropical arbovirus transmitted by female Aedes Aegypti or Aedes Abopitus mosquitos. It is not indigenous to UK but occurs in epidemics in Africa and Asia. It often presents with pyrexia, arthralgia or arthritis, myalgia and a maculopapular rash and can mimic both peripheral and axial inflammatory arthritis as well as more common forms of viral arthritis. It can also become chronic leading to disabling symptoms. The diagnosis should be considered in all patients presenting with early inflammatory arthritis who have travelled to affected areas. Case report - Case description A 57-year-old female developed sudden onset fever along with a macular rash whilst visiting South East Asia. She then developed widespread joint pains and severe inactivity stiffness, particularly affecting her ankles. The rash and fever settled after a few days, but her arthralgia persisted in her cervical spine and both small and large joints. She had a history of recurrent episcleritis and had been investigated for axial spondyloarthropathy two years previously, but MRI imaging of the spine and sacroiliac joints did not show any inflammatory changes. Examination in the rheumatology clinic confirmed right medial epicondylitis, bilateral shoulder tenderness, tenderness over the extensor tendons of the feet and painful cervical spine movement. Investigations revealed high inflammatory markers; CRP 29 (0-10 mg/L) and ESR 48 (0-15 mm/hr), a positive rheumatoid factor but negative anti CCP antibodies and a normal white cell count. Acute seronegative spondyloarthropathy was suspected but Chikungunya serology was requested at the suggestion of the patient, because of the history of a mosquito bite. IgM and IgG antibodies were positive on immunofluorescence, confirming recent infection. She was initially given intramuscular depomedrone and non-steroidal anti-inflammatory drugs (NSAIDs) with a short response but required oral prednisolone 20mg daily to suppress the inflammation in her feet. An MRI confirmed an ankle effusion and peroneal tenosynovitis. After 6 months her symptoms improved, and she was able to stop prednisolone completely and she remains well 9 months after the initial infection. Case report - Discussion Chikungunya infection causes musculoskeletal symptoms in all affected patients, but the clinical presentation can highly variable, from mild joint pain to erosive arthritis. It can be divided into three phases: incubation phase, acute phase, and chronic phase. The incubation phase varies between one to twelve days after the mosquito bite. The acute phase begins with high fever, headache, polyarthralgia/arthritis, lymphadenopathy, and anorexia. Joint involvement is often distal and symmetrical affecting the hands, wrists, shoulders, knees, ankles, and feet. A maculopapular rash is common. Dengue virus and Zika virus infection can present similarly. Treatment for acute Chikungunya fever is supportive. Analgesic, anti-pyretic and NSAIDs are used for symptom relief. During the chronic phase, infected people develop symmetrical, migratory, oligoarticular or polyarticular arthritis with morning stiffness and joint oedema, which can last from months to years. Our patient had a previous history which was consistent with seronegative spondyloarthropathy, an acute presentation of inflammatory arthritis and results and imaging which supported this diagnosis. The correct diagnosis could easily have been missed if a travel history had not been taken and the patient’s suspicions ignored. The best treatment for chronic Chikungunya arthritis is unclear. NSAIDs are often the first treatment but, as in this case systemic steroids are often necessary. Conventional synthetic DMARDs have also been reported efficacious. Biologic DMARDS have been used in resistant cases. Case report - Key learning points Chikungunya has emerged as a global disease affecting millions of people with significant musculoskeletal morbidity. Any patient has travelled to endemic areas including Africa and Asia, with fever and joint pain should be screened for Chikungunya virus as well as Dengue virus, and Zika virus. Diagnosis is either by RT PCR (positive 0-7 days of infection or Immunoglobulin M (detectable after 5 – 10 day of infection and persists for few months). Treatment is supportive in acute phase, may require low doses of steroids to aid resolution of symptoms. Conventional DMARDS have shown benefit in chronic phase with ongoing synovitis/tenosynovitis. Patients may know more about rare, endemic diseases than their European doctors and their suspicions about potential diagnoses should always be considered.