A Young Boy with Deforming Arthropathy

Total Page:16

File Type:pdf, Size:1020Kb

A Young Boy with Deforming Arthropathy Ann Rheum Dis 1998;57:79–80 79 Ann Rheum Dis: first published as 10.1136/ard.57.2.79 on 1 February 1998. Downloaded from LESSON OF THE MONTH A young boy with deforming arthropathy R Handa, P Aggarwal, J P Wali Case report A 15 year old boy presented with a three year history of painless swelling of the proximal interphalangeal (PIP) joints of both the hands. The illness started at the age of 12 years with- out any history of preceding trauma or cold exposure. There was no fever, morning stiV- ness or pain. There was no limitation of hand functions like writing skills, grasping, etc. However, for the past six months, the patient had noticed flexion deformities of the little fin- gers, which could not be corrected. No other joints were involved. The patient was one of three children of a non-consanguinous mar- riage. None of the parents or other siblings had similar illness. The patient had been treated by his doctor for juvenile chronic arthritis with Figure 2 Radiograph of the hands showing epiphyseal diclofenac sodium and low dose prednisone for irregularity of the second phalanx of right and left ring six months without any improvement. General fingers. PIP joints of little fingers are fused. physical and systemic examinations were en- tirely normal. Joint examination showed firm of the proximal epiphyses of the second swelling of the PIP joints. No erythema, local phalanx of right and left ring fingers with rise in temperature or tenderness were noted. fusion of PIP joints of the little fingers. No ero- The fingers showed flexion deformity. No sions were noticed (fig 2). A diagnosis of Thie- http://ard.bmj.com/ Department of shortening was apparent. Active and passive mann’s disease was considered and the patient Medicine, All India movements were normal except in the little reassured with withdrawal of all medications. Institute of Medical fingers, which had a fixed deformity (fig1).All Sciences, New Delhi, other joints of the hand and feet were normal. Discussion India Investigations showed haemoglobin 14.2 R Handa Thiemann’s disease or aseptic necrosis of the × 9 P Aggarwal g/dl, leucocytes 6.1 10 /l ( neutrophils 70%, basal epiphyses of the phalanges of the fingers JPWali lymphocytes 25%, monocytes 3%, eosinophils is a rare condition first described in 1909.1 The 9 2%) and platelets 300 × 10 /l. Westergren principal clinical manifestation is progressive on September 25, 2021 by guest. Protected copyright. Correspondence to: erythrocyte sedimentation rate (ESR) was 5 enlargement of PIP joints of the hands, and of Dr R Handa, Rheumatology Division, Department of mm 1st h. Rheumatoid factor and antinuclear interphalangeal joints of the great toes and Medicine, All India Institute antibodies were negative. Antistreptolysin O occasionally other toes, followed by slight flex- of Medical Sciences, New titres were normal. Blood urea nitrogen, serum ion of the enlarged joints.2 The swelling is gen- Delhi 110029, India. creatinine, serum proteins, aminotransferases erally painless and pain, if present, is usually 3–5 Accepted for publication were within normal limits. Urine analysis was slight and often triggered by cold. The 22 October 1997 normal. Hand radiographs showed irregularity disease typically begins in the prepubertal age group and limitation of function is slight. Most often the disease is transmitted as an autosomal dominant disorder with virtual complete penetrance,34although, sporadic cases are not infrequent.5 The familial disease shows equal sex distribution while sporadic cases show a threefold male dominance.56 Acute phase reactants like erythrocyte sedimentation rate are normal. The proposed clinical criteria4 include onset before the age of 25 and swelling of PIP joints with normal laboratory tests. Radiological fea- tures include irregularity, flattening, fragmen- tation, and broadening of the basal epiphyses of 357 Figure 1 Photograph of the hands. PIP joints are swollen and the fingers show flexion the phalanges. These are later followed by deformity. joint space narrowing, premature epiphyseal 80 Handa, Aggarwal, Wali Table 1 Hand deforming arthropathies in children ease, Kohler’s disease, Osgood-Schlatter’s dis- Ann Rheum Dis: first published as 10.1136/ard.57.2.79 on 1 February 1998. Downloaded from ease, Thiemann’s disease, and Scheuermann’s Condition DiVerential diagnosis disease.9 Juvenile chronic arthritis Pain, swelling, erythema, warmth present in The most important diVerential diagnosis of the aVected joints. ESR and CRP usually Thiemann’s disease is from other inflammatory raised in active disease. Systemic lupus erythematosus Arthropathy is inflammatory, non-erosive, paediatric arthritides like juvenile chronic and most often non-deforming, although arthritis and systemic lupus erythematosus. reversible or fixed deformities may occur. Acute phase reactants are usually, but by no Thiemann’s disease One of the osteochondroses with painless enlargement of PIP joints of hands and feet. means invariably, raised in juvenile chronic Clinical and laboratory features of arthritis while the articular involvement in sys- inflammation absent, ESR normal. temic lupus erythematosus is usually non- Characteristic radiological picture (described in text). deforming. The characteristic age of onset in Diabetic cheiroarthropathy (Rosenbloom Syndrome of insulin dependent diabetes Thiemann’s disease with painless bony en- syndrome) mellitus, short stature and flexion largement of PIP joints without any redness or contractures of finger joints. Pain is typically absent. Functional disability is common. warmth, conspicuous lack of systemic features, Dupuytren’s contracture Nodular thickening of the palmar fascia with and absence of acute phase reactants coupled flexion contractures of the digits. with a benign course make clinical diVerentia- Congenital contractural arachnodactyly Congenital contractures of knees, elbows, and PIP joints, which tend to improve with tion possible. Primary generalised osteoarthri- age. Typically hand and feet are long. tis begins later in life and usually shows less Progressive kyphoscoliosis may develop. symmetrical aVection, without shortening of Traumatic arthropathy Obvious history of trauma present. 4 Frostbite arthropathy History of cold injury present. Distal the phalanges. Other conditions that may phalanges more severely aVected. Sparing of mimic Thiemann’s disease like trauma, infec- thumb characteristic. tion, thermal injury such as frostbite or burns, Burns History of electrical or thermal injury with storage diseases, for example, mucolipidosis prominent skin and soft tissue involvement. Storage diseases, for example, Multiple organ involvement seen in addition III, diabetic cheiroarthropathy, contractural mucopolysaccharidoses to stiVness and deformity of hands, elbows, arachnodactyly, etc, can be easily distinguished and knees. on clinical or radiological grounds51011 (table Sickle cell dactylitis Transient swelling and tenderness of hands and feet seen in children with sickle cell 1). Awareness of this rare disease is important anaemia below 4 years of age. Radiography not only for greater clinical recognition but also reveals periosteal elevation, new avoidance of unnecessary treatment with anti- subperiosteal bone formation, radiolucent areas intermingled with areas of increased inflammatory or disease modifying agents. density (“moth eaten appearance”) Haemochromatosis Degenerative arthropathy involving MP, PIP, DIP joints, hips and knees seen in 20–40% The lesson cases. Rare in children because significant + Deforming arthropathies in children could iron overload takes several years. TB dactylitis Occurs most often in the setting of be caused by juvenile chronic arthritis, sys- pulmonary tuberculosis. Tuberculous temic lupus erythematosus, trauma or thermal arthritis typically involves large joints of injury, diabetic cheiroarthropathy, storage dis- lower limbs. Dactylitis uncommon. eases, contractural arachnodactyly, sickle cell disease, and Dupuytren’s contracture. http://ard.bmj.com/ fusion, and phalangeal shortening. In some + Painless swelling of PIP joints in adolescent cases, radiographic improvement may be seen children, with preserved function and normal because of resorption of bone fragments, but erythrocyte sedimentation rate, should arouse more frequent is the later development of suspicion of Thiemann’s disease. interphalangeal joint osteoarthritis.5 Most often, the disease has a benign course and is 1 Thiemann H. Juvenile epiphysenstorungen. Idiopathische not functionally disabling, although inter- Erkrankung der Epiphysenknorpel der Fingerphalangen. Fortschr Geb Roentgenstr Nuklearmed 1909;14:79–87. on September 25, 2021 by guest. Protected copyright. phalangeal joint osteoarthritis may develop. 2 Molloy MG, Hamilton EBD. Thiemann’s disease. Rheum Thiemann’s disease is now thought to be one Rehabil 1978;17:179–80. 3 Rubinstein HM. Thiemann’s disease. A brief reminder. of the osteochondroses. Osteochondroses are a Arthritis Rheum 1975;18:357–60. group of disorders that share certain features: 4 Allison AC, Blumberg BS. Familial osteoarthropathy of the fingers. J Bone Joint Surg (Br) 1958;40:538–45. predilection for the immature skeleton; in- 5 Melo-Gomes JA, Melo-Gomes E, Viana-Queiros M. volvement of an epiphysis, apophysis, or Thiemann’s disease. J Rheumatol 1981;8:462–7. 6 Gewanter H. Baum J. Thiemann’s disease. J. Rheumatol epiphysioid bone; a radiographic picture that is 1985:12:150–3. dominated by fragmentation, collapse, sclerosis 7 Franck S. Aseptic necrosis in
Recommended publications
  • Juvenile Spondyloarthropathies: Inflammation in Disguise
    PP.qxd:06/15-2 Ped Perspectives 7/25/08 10:49 AM Page 2 APEDIATRIC Volume 17, Number 2 2008 Juvenile Spondyloarthropathieserspective Inflammation in DisguiseP by Evren Akin, M.D. The spondyloarthropathies are a group of inflammatory conditions that involve the spine (sacroiliitis and spondylitis), joints (asymmetric peripheral Case Study arthropathy) and tendons (enthesopathy). The clinical subsets of spondyloarthropathies constitute a wide spectrum, including: • Ankylosing spondylitis What does spondyloarthropathy • Psoriatic arthritis look like in a child? • Reactive arthritis • Inflammatory bowel disease associated with arthritis A 12-year-old boy is actively involved in sports. • Undifferentiated sacroiliitis When his right toe starts to hurt, overuse injury is Depending on the subtype, extra-articular manifestations might involve the eyes, thought to be the cause. The right toe eventually skin, lungs, gastrointestinal tract and heart. The most commonly accepted swells up, and he is referred to a rheumatologist to classification criteria for spondyloarthropathies are from the European evaluate for possible gout. Over the next few Spondyloarthropathy Study Group (ESSG). See Table 1. weeks, his right knee begins hurting as well. At the rheumatologist’s office, arthritis of the right second The juvenile spondyloarthropathies — which are the focus of this article — toe and the right knee is noted. Family history is might be defined as any spondyloarthropathy subtype that is diagnosed before remarkable for back stiffness in the father, which is age 17. It should be noted, however, that adult and juvenile spondyloar- reported as “due to sports participation.” thropathies exist on a continuum. In other words, many children diagnosed with a type of juvenile spondyloarthropathy will eventually fulfill criteria for Antinuclear antibody (ANA) and rheumatoid factor adult spondyloarthropathy.
    [Show full text]
  • Bursae Around the Knee Joints Priyank S Chatra Department of Radiology, Yenepoya Medical College, Mangalore, Karnataka, India
    MUSCULOSKELETAL RADIOLOGY Bursae around the knee joints Priyank S Chatra Department of Radiology, Yenepoya Medical College, Mangalore, Karnataka, India Correspondence: Dr. Priyank S. Chatra, Department of Radiology, Yenepoya Medical College, Deralakatte, Mangalore – 575 018, Karnataka, India. E-mail: [email protected] Abstract A bursa is a fluid-filled structure that is present between the skin and tendon or tendon and bone. The main function of a bursa is to reduce friction between adjacent moving structures. Bursae around the knee can be classified as those around the patella and those that occur elsewhere. In this pictorial essay we describe the most commonly encountered lesions and their MRI appearance. Key words: Iliotibial bursa; infrapatellar bursa; pes anserine bursa Introduction and the gastrocnemius-semimembranosus bursa. On MRI imaging, bursitis appears as an oblong fluid collection in A bursa is a fluid-filled structure that is present between its expected anatomical location. the skin and tendon or tendon and bone. The main function of a bursa is to reduce friction between adjacent Prepatellar Bursitis moving structures. Typically, bursae are located around large joints such as the shoulder, knee, hip, and elbow.[1] The prepatellar bursa is located between the patella and the Inflammation of this fluid-filled structure is called bursitis. overlying subcutaneous tissue. Chronic trauma in the form Trauma, infection, overuse, and hemorrhage are some of prolonged or repeated kneeling leads to inflammation of the common
    [Show full text]
  • 'Dialysis Related Arthropathy': a Survey of 95 Patients Receiving Chronic Haemodialysis with Special Reference to 132 Microglobulin Related Amyloidosis
    Ann Rheum Dis: first published as 10.1136/ard.48.5.409 on 1 May 1989. Downloaded from Annals of the Rheumatic Diseases, 1989; 48, 409-420 'Dialysis related arthropathy': a survey of 95 patients receiving chronic haemodialysis with special reference to 132 microglobulin related amyloidosis N P HURST,' R VAN DEN BERG,' A DISNEY,2 M ALCOCK,3 L ALBERTYN,3 M GREEN,' AND V PASCOE4 From the 'Rheumatology Unit, the 2Renal Unit, the 3Department of Radiology, and the 4Department of Pathology, The Queen Elizabeth Hospital, Woodville, South Australia SUMMARY Ninety five patients receiving chronic haemodialysis (CHD) were surveyed to determine the prevalence of rheumatic disease and, where possible, its aetiology. At least three distinct rheumatic syndromes were identified-a group of patients with a syndrome consisting of large and medium joint synovial swelling, restricted hips and shoulders, tenosynovitis, carpal tunnel syndrome, and bone cysts due to deposition of 132 microglobulin related amyloid (AMP2m); a second group with erosive azotaemic osteoarthropathy; and a third group with age related degenerative disease of small, large, and axial joints. The data presented suggest that in patients receiving CHD (a) the prevalence of AM2i2m deposition and the associated syndrome increases with duration of dialysis, but in patients who have been dialysed for more than 10 years the risk of developing AM2n2m is related to age; (b) AM2i2m deposition in subchondral cysts, but not synovium, causes joint destruction; also, AMp2m may be more prone to deposition in synovium of joints already damaged by other processes; (c) in the absence of synovial iron deposition synovial AM2n2m is not associated with an inflammatory infiltrate; (d) hyperparathyroidism and perhaps other factors such as synovial iron deposition are probably more important than AMgi2m as causes http://ard.bmj.com/ of peripheral joint degeneration and destructive spondyloarthropathy in patients receiving CHD.
    [Show full text]
  • Rotator Cuff and Subacromial Impingement Syndrome: Anatomy, Etiology, Screening, and Treatment
    Rotator Cuff and Subacromial Impingement Syndrome: Anatomy, Etiology, Screening, and Treatment The glenohumeral joint is the most mobile joint in the human body, but this same characteristic also makes it the least stable joint.1-3 The rotator cuff is a group of muscles that are important in supporting the glenohumeral joint, essential in almost every type of shoulder movement.4 These muscles maintain dynamic joint stability which not only avoids mechanical obstruction but also increases the functional range of motion at the joint.1,2 However, dysfunction of these stabilizers often leads to a complex pattern of degeneration, rotator cuff tear arthropathy that often involves subacromial impingement.2,22 Rotator cuff tear arthropathy is strikingly prevalent and is the most common cause of shoulder pain and dysfunction.3,4 It appears to be age-dependent, affecting 9.7% of patients aged 20 years and younger and increasing to 62% of patients of 80 years and older ( P < .001); odds ratio, 15; 95% CI, 9.6-24; P < .001.4 Etiology for rotator cuff pathology varies but rotator cuff tears and tendinopathy are most common in athletes and the elderly.12 It can be the result of a traumatic event or activity-based deterioration such as from excessive use of arms overhead, but some argue that deterioration of these stabilizers is part of the natural aging process given the trend of increased deterioration even in individuals who do not regularly perform overhead activities.2,4 The factors affecting the rotator cuff and subsequent treatment are wide-ranging. The major objectives of this exposition are to describe rotator cuff anatomy, biomechanics, and subacromial impingement; expound upon diagnosis and assessment; and discuss surgical and conservative interventions.
    [Show full text]
  • Treatment of Established Volkmann's Contracture*
    ~hop. Acta Treatment of Established Volkmann’sContracture* BY KENYA TSUGE, M.D.’J’, HIROSHIMA, JAPAN ldon, From the Department of Orthopaedic Surgery, Hiroshima Universi~.’ 1-76, School of Medicine, Hiroshima 38. The disease first described by Volkmann in 1881 is the extent of the disease: mild, moderate, and severe. In generally considered to result from spasm of the main ar- the mild type, also called the localized type, there was de- ~ts of teries of the forearm, and their branches as a consequence generation of part of the flexor digitorum profundus mus- Acta of trauma to the elbow or forearm. The severe and pro- cle, causing contractures in only two or three fingers. longed but incomplete interruption of arterial blood sup- There were hardly any neurological signs, and when pres- ~. (in ply, together with venostasis, produces acute ischemic ent they were minimum. In the moderate type, the muscle z and necrosis of the flexor muscles. The most marked ischemia degeneration involved all or nearly all of the flexor digito- occurs in the deeply situated muscles such as the flexor rum profundus and flexor pollicis longus, with partial pollicis longus and flexor digitorum profundus, but severe degeneration of the superficial muscles as well. The neu- ischemia is evident in the pronator teres and flexor rological signs were invariably present and generally -484, digitorum superficialis muscles, and comparatively mild the median nerve was more severely affected than the :rtag, ischemia occurs in the superficially located muscles such ulnar nerve. In the severe type, there was degeneration as the wrist flexors. The muscle degeneration which fol- of all the flexor muscles with necrosis in the center ).
    [Show full text]
  • Rotator Cuff Tear Arthropathy: Pathophysiology, Diagnosis And
    yst ar S em ul : C c u s r u r e M n t & R Orthopedic & Muscular System: c e Aydin, et al., Orthopedic Muscul Syst 2014, 3:2 i s d e e a p ISSN: 2161-0533r o c DOI: 10.4172/2161-0533-3-1000159 h h t r O Current Research Review Article Open Access Rotator Cuff Tear Arthropathy: Pathophysiology, Diagnosis and Treatment Nuri Aydin*, Okan Tok and Bariş Görgün Istanbul University Cerrahpaşa, School of Medicine, Istanbul, Turkey *Corresponding author: Nuri Aydin, Istanbul University Cerrahpaşa, School of Medicine, Orthopaedics and Traumatology, Istanbul, Turkey, Tel: +905325986232; E- mail: [email protected] Rec Date: Jan 25, 2014, Acc Date: Mar 22, 2014, Pub Date: Mar 28, 2014 Copyright: © 2014 Aydin N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract The term rotator cuff tear arthropathy is a broad spectrum pathology but it involves common characteristic features as rotator cuff tear, leading to glenohumeral joint arthritis and superior migration of the humeral head. Although there are several factors described causing rotator cuff tear arthropathy, the exact mechanism is still unknown because the rotator cuff tear arthropathy develops in only a group of patients with chronic rotator cuff tear. The aim of this article is to review pathophysiology of rotator cuff tear arthropathy, to explain the diagnostic features and to discuss the management of the disease. Keywords: Arthropathy; Glenohumeral joint; Articular fluid Rotator cuff tear not only plays a role at the beginning of the disease, but also a developed rotator cuff tear is a result of the inflammatory Introduction process.
    [Show full text]
  • CPT® Procedural Coding 110 L with Areportoftheprocedure
    20610-20611 2017 Illustrated Coding and Billing Expert for Orthopedics Lower 20610-20611 ICD-9-CM Diagnostic Codes M16.7 Other unilateral secondary 711.05 Pyogenic arthritis involving pelvic osteoarthritis of hip 20610 Arthrocentesis, aspiration and/or region and thigh M17.0 Bilateral primary osteoarthritis of injection, major joint or bursa (eg, 711.06 Pyogenic arthritis involving lower leg knee shoulder, hip, knee, subacromial 713.5 Arthropathy associated with ⇄ M17.11 Unilateral primary osteoarthritis, right bursa); without ultrasound guidance neurological disorders knee 20611 Arthrocentesis, aspiration and/or 714.0 Rheumatoid arthritis ⇄ M17.12 Unilateral primary osteoarthritis, left knee injection, major joint or bursa (eg, 715.15 Osteoarthrosis, localized, primary, pelvic region and thigh M17.2 Bilateral post-traumatic osteoarthritis shoulder, hip, knee, subacromial 715.16 Osteoarthrosis, localized, primary, of knee bursa); with ultrasound guidance, with lower leg M17.5 Other unilateral secondary permanent recording and reporting 715.25 Osteoarthrosis, localized, secondary, osteoarthritis of knee (Do not report 20610, 20611 in pelvic region and thigh ⇄ M1A.051 Idiopathic chronic gout, right hip conjunction with 27370, 76942) 715.26 Osteoarthrosis, localized, secondary, ⇄ M1A.062 Idiopathic chronic gout, left knee (If fluoroscopic, CT, or MRI guidance is lower leg ⇄ M25.052 Hemarthrosis, left hip ⇄ M25.061 Hemarthrosis, right knee performed, see 77002, 77012, 77021) 715.35 Osteoarthrosis, localized, not specified whether primary
    [Show full text]
  • Current Trends in Tendinopathy Management
    Best Practice & Research Clinical Rheumatology 33 (2019) 122e140 Contents lists available at ScienceDirect Best Practice & Research Clinical Rheumatology journal homepage: www.elsevierhealth.com/berh 8 Current trends in tendinopathy management * Tanusha B. Cardoso a, , Tania Pizzari b, Rita Kinsella b, Danielle Hope c, Jill L. Cook b a The Alphington Sports Medicine Clinic, 339 Heidelberg Road, Northcote, Victoria, 3070, Australia b La Trobe University Sport and Exercise Medicine Research Centre, La Trobe University, Corner of Plenty Road and Kingsbury Drive, Bundoora, Victoria, 3083, Australia c MP Sports Physicians, Frankston Clinic, Suite 1, 20 Clarendon Street, Frankston, Victoria, 3199, Australia abstract Keywords: Tendinopathy Tendinopathy (pain and dysfunction in a tendon) is a prevalent Management clinical musculoskeletal presentation across the age spectrum, Rehabilitation mostly in active and sporting people. Excess load above the ten- Achilles tendinopathy don's usual capacity is the primary cause of clinical presentation. Rotator cuff tendinopathy The propensity towards chronicity and the extended times for recovery and optimal function and the challenge of managing tendinopathy in a sporting competition season make this a difficult condition to treat. Tendinopathy is a heterogeneous condition in terms of its pathology and clinical presentation. Despite ongoing research, there is no consensus on tendon pathoetiology and the complex relationship between tendon pathology, pain and func- tion is incompletely understood. The diagnosis of tendinopathy is primarily clinical, with imaging only useful in special circum- stances. There has been a surge of tendinopathy treatments, most of which are poorly supported and warrant further exploration. The evidence supports a slowly progressive loading program, rather than complete rest, with other treatment modalities used as adjuncts mainly targeted at achieving pain relief.
    [Show full text]
  • Pigmented Villonodular Synovitis in Pediatric Population: Review of Literature and a Case Report Mohsen Karami*, Mehryar Soleimani and Reza Shiari
    Karami et al. Pediatric Rheumatology (2018) 16:6 DOI 10.1186/s12969-018-0222-4 CASEREPORT Open Access Pigmented villonodular synovitis in pediatric population: review of literature and a case report Mohsen Karami*, Mehryar Soleimani and Reza Shiari Abstract Background: Pigmented villonodular synovitis (PVNS) is a rare proliferative process in children that mostly affects the knee joint. Case Presentation: The study follows the case of a 3-year-old boy presenting recurrent patellar dislocation and PVNS. Due to symptoms such as chronic arthritis, he had been taking prednisolone and methotrexate for 6 months before receiving a definitive diagnosis. After a period of showing no improvements from his treatment, he was referred to our center and was diagnosed with local PVNS using magnetic resonance imaging (MRI). The patient was treated for his patellar dislocation by way of open synovectomy, lateral retinacular release, and a proximal realignment procedure, with no recurrence after a 24-month follow-up. Conclusion: PVNS may appear with symptoms resembling juvenile idiopathic arthritis, thus the disease should be considered in differential diagnosis of any inflammatory arthritis in children. PVNS may also cause mechanical symptoms such as patellar dislocation. In addition to synovectomy, a realignment procedure can be a useful method of treatment. Keywords: Juvenile idiopathic arthritis, Patellar dislocation, Pigmented villonodular synovitis Background aberrations that cause hemorrhagic tendencies, as well as Pigmented villonodular synovitis (PVNS) is a rare prolif- genetic factors, have been proposed as potential causes erative process that affects the synovial joint, tendon [2, 3]. Trauma and rheumatoid arthritis association have sheaths, and bursa membranes [1]. The estimated inci- also been considered [14, 15, 33].
    [Show full text]
  • Calcified Tendinitis: a Review
    Ann Rheum Dis: first published as 10.1136/ard.42.Suppl_1.49 on 1 January 1983. Downloaded from Ann Rheum Dis (1983), 42, Supplement p 49 Calcified tendinitis: a review G. FAURE,' G. DACULSI2 From the 'Clinique Rhumatologique et Laboratoire d'immunologie, Faculte A de Medecin, Universite de Nancy I, 54500 Vandoeuvre les Nancy, France and 2U225 INSERM, Faculte de Chirurgie Dentaire, Place Alexis Ricordeau, 44042 Nantes, France Introduction Calcified tendinitis in clinical practice Calcified tendinitis is a common CLINICAL FEATURES disorder. Many names have been used According to Welfling calcific to describe it: some of them, such as periarthritis is responsible for 7% of 'calcific periarthritis', emphasise the painful shoulder syndromes,' which extra-articular site of the deposit; have various presentations. others, such as 'periarticular apatite (1) Chronic symptoms-more or deposition', mention the nature of the less severe pain; tenderness leading to compound found in the calcification; various degrees of incapacitation. and more recent ones, such as These symptoms induce the demand 'calcifying tendinitis',-'3 emphasise the. for radiographs, which reveal the Fig. 1 Calcific periarthritis ofthe active process that might explain the presence of deposits. shoulder. Calcification is obvious; it deposition. Differentiated from (2) Acute inflammatory crisis with has already migrated from copyright. arthritis at the end of the nineteenth severe pain, tenderness, and local supraspinatus region to bursa area. century, this syndrome has only oedematous inflammation sometimes recently been related to the presence leading to restricted active an*d passive of apatite in tendon sheaths.4'5 It can motion. Fever and malaise may be affect almost any tendon at its observed.
    [Show full text]
  • Table of Contents 1
    GENERAL THORACIC SURGERY DATABASE v.2.3 TRAINING MANUAL August 2017 Table of Contents 1. Demographics ................................................................................................................................................................. 2 2. Follow Up ........................................................................................................................................................................ 9 3. Admission ..................................................................................................................................................................... 10 4. Pre-Operative Evaluation ............................................................................................................................................. 14 5. Diagnosis (Category of Disease) ................................................................................................................................... 48 6. Procedure ..................................................................................................................................................................... 70 7. Post-Operative Events ................................................................................................................................................ 111 8. Discharge .................................................................................................................................................................... 135 9. Quality Measures ......................................................................................................................................................
    [Show full text]
  • Trauma and Reiter's Syndrome: Development of 'Reactive Arthropathy' in Two Patients Following Musculoskeletal Injury
    Ann Rheum Dis: first published as 10.1136/ard.43.6.829 on 1 December 1984. Downloaded from Annals of the Rheumatic Diseases, 1984, 43, 829-832 Trauma and Reiter's syndrome: development of 'reactive arthropathy' in two patients following musculoskeletal injury JEFFREY J. WISNIESKI From the Medical Service, Rheumatology Section, Cleveland Veterans Administration Medical Center, and Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. SUMMARY Two patients are reported who developed arthropathies with some features of Reiter's syndrome shortly after physical injury. Both were HLA-B27 positive. No other precipitating factors were identified, and the possibility that trauma may have precipitated a reactive arth- ropathy is discussed. Key words: endogenous antigen (immunogen), genetic predisposition, collagen. copyright. Concepts of Reiter's syndrome (RS) have changed swelling, pain, and heat; internal mechanical dramatically in the past decade. Notable develop- derangement was suspected. Five months after the ments include: (1) recognition that clinical activity trauma arthroscopy revealed hyperaemic and thick- may be acute/self-limited, acute/recurrent, or ened synovium but no structural abnormality. Syno- chronic'-5; (2) recognition that disease mani- vial biopsy showed chronic synovitis with marked festations vary from 'incomplete' RS to multisystem lymphocyte and plasma cell infiltration. involvement'-3; (3) development of concepts of Seven months after the injury the knee continued genetic predisposition and linkage4 5; and (4) charac- to be warm and painful, with thickened synovium and http://ard.bmj.com/ terisation of RS as reactive arthritis developing in a large effusion. No other joints were involved. Con- genetically predisposed individuals.45 In most junctivitis of the left eye was noted.
    [Show full text]