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Physical Examination of the Hand
Published in J. Terrence Jose Jerome, Clinical Examination of the Hand, 2022
When the central slip is injured or incompetent, it is possible to generate extensor force at the DIP joint with maximal passive PIP joint flexion, which is the basis of the Elson test for detecting acute central slip rupture. As described by Elson, the examiner passively flexes the PIP joint 90° to the tabletop and asks the patient to attempt active extension of the PIP joint while the examiner resists PIP joint extension. When acute rupture of the central slip occurs, no extension power is felt at the PIP joint but significant extension power, or hyperextension, is produced at the DIP joint. This test has been found to be the most sensitive physical examination test to detect acute central slip rupture (Video 3.9).Swan-neck deformity
Questions
Published in Thomas Hester, Iain MacGarrow, Surgical SBAs for Finals with Explanatory Answers, 2018
Which joint is hyperextended in Swan neck deformity? Proximal interphalangeal jointMetacarpophalangeal jointDistal interphalangeal jointRadial deviationUlnar deviation
Hand trauma
Published in Sebastian Dawson-Bowling, Pramod Achan, Timothy Briggs, Manoj Ramachandran, Stephen Key, Daud Chou, Orthopaedic Trauma, 2014
Volar plate rupture often results from hyperextension injury and is frequently missed. Volar tenderness or dorsal PIPJ subluxation on lateral radiograph should raise suspicion. If the injury is well reduced, management in an extension block splint with neighbour strapping may be followed by early mobilization.A swan neck deformity may result.
Volar transfer of the lateral band with transverse retinacular ligament is effective for the correction of swan-neck deformity caused by volar plate injury of the PIP joint
Published in Modern Rheumatology Case Reports, 2020
Masahiro Sato, Taku Suzuki, Takuji Iwamoto, Noboru Matsumura, Hiroo Kimura, Kazuki Sato, Masaya Nakamura, Morio Matsumoto
Volar plate injury leads to hyperextension of the proximal interphalangeal (PIP) joint. Continuous hyperextension of the PIP joint sometimes causes swan-neck deformity of the affected finger. To date, a variety of surgical options and modified original techniques for the correction of swan-neck deformity have been reported: dermodesis (Figure 1(A)) [1], direct repair of the volar plate (Figure 1(B)) [2], tenodesis with a flexor digitorum superficialis (FDS) slip (Figure 1(C)) [3], reconstruction of the volar plate with the palmaris longus (PL) tendon (Figure 1(D)) [4], spiral oblique retinacular ligament reconstruction (ORL) with intrinsic release (Figure 1(E)) [5,6], reattachment of the collateral ligament (Figure 1(F)) [7], or lateral band mobilisation (Figure 1(G)) [1]. Most of the original literature on this topic is more than 40–60 years old. Although these methods showed satisfactory results, surgery on the volar mechanism (volar plate, flexor tendon or tendon sheath) or release of the lateral band is rather invasive. We introduce a technique with volar transfer of the lateral band using the transverse retinacular ligament for swan-neck deformity caused by volar plate injury of the PIP joint.
Simultaneous development of cutaneous vasculitis and an autoimmune bullous skin disease during anti-TNF therapy for rheumatoid arthritis: a case report and review of the literature
Published in Modern Rheumatology Case Reports, 2018
Yamato Nakamura, Koichiro Ohmura, Teruki Dainichi, Nobuo Kuramoto, Yuto Nakakubo, Yusuke Takeuchi, Shuji Akizuki, Kosaku Murakami, Ran Nakashima, Hajime Yoshifuji, Wataru Nishie, Kentaro Izumi, Hiroshi Shimizu, Motomu Hashimoto, Masao Tanaka, Takaki Sakurai, Akihiko Kitoh, Tsuneyo Mimori
The patient was taking multiple medications, including furosemide, bisoprolol, nicorandil, cilostazol, bayaspirin, losartan, lansoprazole and acetaminophen, for an extended period. Physical examination revealed swan neck deformity of the digits and ankylosis of the hand joints. No joint swelling or tenderness was observed. Dermatologically, we noted annular erythema and small blisters bilaterally on the thighs, and palpable purpura and multiple blisters bilaterally on the lower legs. Eruption and blisters were also seen on the DIP area of the right third finger. In addition, both of the elbows and heels were ulcerative. Rheumatoid nodules were not found in this patient. Representative images of the skin manifestations are shown in Figure 1. Neurological examination revealed no special abnormalities. A blood test showed: WBC 5530/µL, Hb 7.3 mg/dL, Reticulocyte 28.5‰, Plt 37.5 × 104/µL, ESR 146 mm/h, APTT 37.3 sec., Fib 519 mg/dL, D-dimer 5.4 µg/mL, Alb 2.5 g/dL, TP 6.9 g/dL, Cre 0.99 mg/dL, BUN 39 mg/dL, CRP 3.3 mg/dL, BNP 1107.9 pg/mL, C3 120.8 mg/dL, C4 19.4 mg/dL, CH50 55 U/mL. Both rheumatoid factor (359.5 U/mL) and anti-CCP antibody (1950 U/mL) were elevated. The following autoantibodies were negative: MPO-ANCA, PR3-ANCA, Anti-nuclear antibody, anti-SS-A antibody and immune complex (C1q). On the chest X ray, we noted lobar consolidation bilaterally on the lower lung field. After admission, skin biopsies were performed from (1) the ulcer edge and (2) the blister lesion. Specimen (1) showed infiltration of eosinophils and neutrophils into the superficial layer of the dermis, nuclear dust and fibrinoid degeneration around capillaries, indicating leucocytoclastic vasculitis (LCV, Figure 2(A,B)), consistent with the findings at the former hospital. Specimen (2) showed infiltration of eosinophils and neutrophils into the dermis beneath a subepidermal bulla, as well as nuclear dust (Figure 2(C,D)). Immunofluorescence analysis showed linear IgG and C3 deposits in the basement membrane zone (Figure 2(E,F)). For further classification, we conducted ELISA for full-length BP180 and BP230, and Western blotting of anti-laminin γ1 antibody using the patient’s serum; however, all antibodies to these autoantigens were negative (data not shown). Indirect immunofluorescence analysis of human salt-split skin was also negative (data not shown). Based on these findings, we concluded that these skin manifestations are a combination of LCV and a pemphigoid disease without detectable circulating autoantibodies. ETN injection was suspended, iguratimod was discontinued and we started the treatment with methylprednisolone 16 mg/day and continued salazosulfapyridine (SASP) 1000 mg/day because SASP had been administered for more than 8 years throughout her clinical course. Several weeks later, skin blisters and eruptions began to improve. During tapering of glucocorticoids, we added nicotinamide and doxycycline for further treatment of blistering lesions. As a result, 4 months after admission, blisters had disappeared with slight pigmentation on the lower limbs. The clinical course of the patient is summarised in Figure 3.