Guidelines for the Management of Acute Joint Bleeds and Chronic Synovitis in Haemophilia a United Kingdom Haemophilia Centre Doctors’ Organisation (UKHCDO) Guideline

Total Page:16

File Type:pdf, Size:1020Kb

Guidelines for the Management of Acute Joint Bleeds and Chronic Synovitis in Haemophilia a United Kingdom Haemophilia Centre Doctors’ Organisation (UKHCDO) Guideline Haemophilia (2017), 1–10 DOI: 10.1111/hae.13201 REVIEW ARTICLE Guidelines for the management of acute joint bleeds and chronic synovitis in haemophilia A United Kingdom Haemophilia Centre Doctors’ Organisation (UKHCDO) guideline J. HANLEY,* A. MCKERNAN,† M. D. CREAGH,‡ S. CLASSEY,§ P. MCLAUGHLIN,¶ N. GODDARD,¶ P. J. BRIGGS,* S. FROSTICK,** P. GIANGRANDE,†† J. WILDE,‡‡ J. THACHIL§§ and P. CHOWDARY¶ ON BEHALF OF THE MUSCULOSKELETAL WORKING PARTY OF THE UKHCDO *Haemophilia Centre, Royal Victoria Infirmary, Newcastle upon Tyne; †Department of Haematology, Derby Hospitals NHS Foundation Trust, Derby; ‡Haemophilia Centre, Royal Cornwall Hospitals NHS Trust, Truro; §Haemophilia Centre, Guys and St. Thomas’ NHS Foundation Trust, London; ¶Katharine Dormandy Haemophilia and Thrombosis Centre, Royal Free Hospital, London; **Institute of Translational Medicine, University of Liverpool, Liverpool; ††Haemophilia Centre, Churchill Hospital, Oxford; ‡‡Haemophilia Centre, Queen Elizabeth Hospital Birmingham, Birmingham; and §§Haemophilia Centre, Manchester Royal Infirmary, Manchester, UK Keywords: arthropathy, haemarthrosis, haemophilia, radioactive synovectomy, synovitis Introduction Although the exact pathogenesis of haemophilic arthropathy has not been elucidated, several in vitro ani- Prior to the availability of clotting factor concentrates, mal and human experiments have demonstrated blood- the natural history of arthropathy in severe haemophilia induced changes in all the ‘components’ of large synovial was well described, with recurrent bleeds into joints joints including the synovium itself, cartilage and the leading to progressive joint damage and ultimate subchondral bone. The two major changes in the syn- destruction with associated functional problems. The ovium are hypertrophy and hypervascularity. The key prophylactic use of factor concentrates has dramatically stimulant for these changes is iron released into the syn- modified the natural history of haemophilic arthropa- ovial fluid, which is both pro-inflammatory and proan- thy. The early use of prophylaxis can prevent joint giogenic [2–4]. The consequence of neovascularisation bleeding and avoid the cycle of damage associated with in the synovium is predisposition to more bleeding since recurrent haemarthrosis. Children who are treated on these new vessels are friable. This leads to a vicious circle prophylaxis schedules often reach skeletal maturity of bleeding, iron accumulation, synovial hypertrophy with well-preserved joint function. However, in addi- and hypervascularization leading to further bleeding tion to the clinically obvious bleeds, recurrent subclini- and ultimately progressive joint damage. Interventions cal episodes may also contribute to joint damage [1]. aimed at preventing or breaking this cycle are key strate- Once joint arthropathy is established, prophylactic gies for the preservation of joint function in people with treatment may not prevent further joint deterioration. haemophilia. Bleeding is particularly problematic in the diarthrodial-hinged joints such as the knee, elbow and ankle. It is therefore important that acute bleeds in Correspondence: John Hanley, Haemophilia Centre, Royal Vic- patients on either ‘on demand’ or ‘prophylaxis’ regimens toria Infirmary, Queen Victoria Road, Newcastle upon Tyne are treated optimally with the aim of minimizing the NE1 4LP, UK. synovial proliferation secondary to bleeding which is Tel.: 0191 282 4159; fax: 0191 282 0814; central to the pathogenesis of arthropathy. e-mail: [email protected] A recent survey has shown significant variation in Accepted after revision 24 January 2017 practice in the UK [5], which suggests that there is a © 2017 John Wiley & Sons Ltd 1 2 J. HANLEY et al. need for guidelines as a framework for best practice. The objective of initial factor replacement therapy is Evidence-based guidelines were developed summariz- to improve haemostasis in order to arrest bleeding. ing best practice for the assessment and management Subsequent treatment aims to prevent recurrent bleed- of acute joint bleeds and chronic synovitis in persons ing and the onset and progression of joint damage. with haemophilia. This guideline does not include sur- Prompt treatment of bleeding is important and as it gical procedures such as surgical synovectomy, has the advantage of potentially preventing permanent arthrodesis and arthroplasty. damage and this is best achieved with home therapy and patients have been traditionally advised to treat Materials and methods any early symptoms and signs of bleeding. The advan- tages of home therapy include significant decreases in The information contained in this guideline was days lost from work and school, days hospitalized and gathered from an appropriate and pertinent literature hospital visits [8]. In those with established arthropa- search in relation to UK practice. The writing group thy, it may be difficult to distinguish early bleeds from produced the draft guideline, which was subsequently flares of arthritic pain [9,10]. revised by consensus by members of the United Kingdom Haemophilia Centre Doctors’ Organisation Haemostatic management of patients with (UKHCDO) Advisory Board. The ‘GRADE’ system Haemophilia A and B was used to quote levels and grades of evidence, details of which can be found at: http://www. Dose of initial therapy. Early bleeds in patients who gradeworkinggroup.org. Strong recommendations are on prophylaxis are usually adequately treated by a (grade 1, ‘recommended’) are made when there is single dose with resumption of usual prophylaxis there- confidence that the benefits either do or do not out- after. Early studies attempted to investigate the opti- weigh the harm and costs of treatment. Where the mum treatment for bleed resolution. The interpretation magnitude of benefit or not is less certain, a weaker of these studies is complicated by the variable severity grade 2 recommendation (‘suggested’) is made. Grade of the bleeds included and the lack of standardized 1 recommendations can be applied uniformly to assessment criteria. Prior to the availability of factor most patients, whereas grade 2 recommendations concentrates, it was demonstrated that doses of cryo- require a more individualized application. The qual- precipitate achieving FVIII plasma levels of 28%, 35% ity of evidence is graded as high (A), based on high and 53% correlated with successful treatment in 90%, quality randomized clinical trials, moderate (B), low 95% and 99% of bleeding episodes respectively [11]. (C) or very low (D). Many early studies demonstrated that prompt, low doses of factor were equally effective in resolution of Management of acute haemarthrosis bleeds [12–14] but more rapid improvements were demonstrated with higher factor levels [15]. Prophylaxis is the current standard of care, although There are few randomized trials which have com- individual patients continue with on-demand treat- pared different initial doses of factor. One study found ment [6]. In patients receiving on-demand treatment, À that an initial treatment with factor VIII 28 IU kg 1 spontaneous and traumatic bleeds are common [7]. À was no more effective than 14 IU kg 1 in terms of For those receiving prophylaxis, trauma is often the time to symptom resolution and requirement for fur- major precipitant of bleeding but inadequate trough ther treatment [16]. However, the beneficial effect of levels, missed doses, underlying synovitis or estab- a higher initial dose has been demonstrated where lished joint damage may be contributory factors. The patients with levels of 40% compared to 20% had signs and symptoms associated with joint bleeds are shorter time to full functional recovery [17]. Pivotal shown in Table 1. A re-bleed is defined as worsening studies of recombinant factor VIII and Factor IX con- of the condition either on treatment or within 72 h centrates, including studies of extended half-life after stopping treatment [7]. Table 1. Symptoms and signs of joint bleeds. Bleed type Symptoms Signs References Early bleed A sensation of fullness, stiffness, Normal motion [7,73] discomfort, pain or tingling at the end of range of movement in the absence of trauma. Often described as aura by patients and at times can be difficult to distinguish from arthritic pain Moderate Pain Some swelling. Restriction of movement Severe Severe pain Marked swelling. Almost complete restriction [11] of movement ‘Joint immobilizing bleeds’ [16] Haemophilia (2017), 1--10 © 2017 John Wiley & Sons Ltd JOINT BLEEDS AND SYNOVITIS IN HAEMOPHILIA 3 products, have shown variation in the doses used, and there is inadequate response in the first 36 to 48 h the median dose used for bleed resolution was around (1C). À 30 IU Kg 1 in most studies, with 90 to or -95% of the bleeds requiring one or two infusions for complete Haemostatic management of patients with resolution [12,18–21]. In a retrospective study factor, À inhibitors to Factor VIII and IX doses of 25 to –40 IU kg 1 per bleeding episode were inferior only to prophylaxis in terms of reducing the Patients with inhibitors do not necessarily have an progression of arthropathy [22]. increased frequency of spontaneous joint and soft tissue bleeds compared to non-inhibitor patients but do have Subsequent factor treatment. Subsequent factor ther- a higher tendency to develop target joints, which can apy depends on the severity of the bleed. Serial ultra- be difficult to manage. Many inhibitor patients are now sounds of joint bleeds show a persistent effusion for a well established
Recommended publications
  • WFH Treatment Guidelines 3Ed Chapter 7 Treatment Of
    96 TREATMENT OF SPECIFIC 7 HEMORRHAGES Johnny Mahlangu1 | Gerard Dolan2 | Alison Dougall3 | Nicholas J. Goddard4 | Enrique D. Preza Hernández5 | Margaret V. Ragni6 | Bradley Rayner7 | Jerzy Windyga8 | Glenn F. Pierce9 | Alok Srivastava10 1 Department of Molecular Medicine and Haematology, University of the Witwatersrand, National Health Laboratory Service, Johannesburg, South Africa 2 Guy’s and St. Thomas’ Hospitals NHS Foundation Trust, London, UK 3 Special Care Dentistry Division of Child and Public Dental Health, School of Dental Science, Trinity College Dublin, Dublin Dental University Hospital, Dublin, Ireland 4 Department of Trauma and Orthopaedics, Royal Free Hospital, London, UK 5 Mexico City, Mexico 6 Division of Hematology/Oncology, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA 7 Cape Town, South Africa 8 Department of Hemostasis Disorders and Internal Medicine, Laboratory of Hemostasis and Metabolic Diseases, Institute of Hematology and Transfusion Medicine, Warsaw, Poland 9 World Federation of Hemophilia, Montreal, QC, Canada 10 Department of Haematology, Christian Medical College, Vellore, India All statements identified as recommendations are • In general, the main treatment for bleeding episodes in consensus based, as denoted by CB. patients with severe hemophilia is prompt clotting factor replacement therapy and rehabilitation. However, different types of bleeds and bleeding at particular anatomical sites 7.1 Introduction may require more specific management with additional
    [Show full text]
  • 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]
  • Familial Multiple Coagulation Factor Deficiencies
    Journal of Clinical Medicine Article Familial Multiple Coagulation Factor Deficiencies (FMCFDs) in a Large Cohort of Patients—A Single-Center Experience in Genetic Diagnosis Barbara Preisler 1,†, Behnaz Pezeshkpoor 1,† , Atanas Banchev 2 , Ronald Fischer 3, Barbara Zieger 4, Ute Scholz 5, Heiko Rühl 1, Bettina Kemkes-Matthes 6, Ursula Schmitt 7, Antje Redlich 8 , Sule Unal 9 , Hans-Jürgen Laws 10, Martin Olivieri 11 , Johannes Oldenburg 1 and Anna Pavlova 1,* 1 Institute of Experimental Hematology and Transfusion Medicine, University Clinic Bonn, 53127 Bonn, Germany; [email protected] (B.P.); [email protected] (B.P.); [email protected] (H.R.); [email protected] (J.O.) 2 Department of Paediatric Haematology and Oncology, University Hospital “Tzaritza Giovanna—ISUL”, 1527 Sofia, Bulgaria; [email protected] 3 Hemophilia Care Center, SRH Kurpfalzkrankenhaus Heidelberg, 69123 Heidelberg, Germany; ronald.fi[email protected] 4 Department of Pediatrics and Adolescent Medicine, University Medical Center–University of Freiburg, 79106 Freiburg, Germany; [email protected] 5 Center of Hemostasis, MVZ Labor Leipzig, 04289 Leipzig, Germany; [email protected] 6 Hemostasis Center, Justus Liebig University Giessen, 35392 Giessen, Germany; [email protected] 7 Center of Hemostasis Berlin, 10789 Berlin-Schöneberg, Germany; [email protected] 8 Pediatric Oncology Department, Otto von Guericke University Children’s Hospital Magdeburg, 39120 Magdeburg, Germany; [email protected] 9 Division of Pediatric Hematology Ankara, Hacettepe University, 06100 Ankara, Turkey; Citation: Preisler, B.; Pezeshkpoor, [email protected] B.; Banchev, A.; Fischer, R.; Zieger, B.; 10 Department of Pediatric Oncology, Hematology and Clinical Immunology, University of Duesseldorf, Scholz, U.; Rühl, H.; Kemkes-Matthes, 40225 Duesseldorf, Germany; [email protected] B.; Schmitt, U.; Redlich, A.; et al.
    [Show full text]
  • Synovial Fluidfluid 11
    LWBK461-c11_p253-262.qxd 11/18/09 6:04 PM Page 253 Aptara Inc CHAPTER SynovialSynovial FluidFluid 11 Key Terms ANTINUCLEAR ANTIBODY ARTHROCENTESIS BULGE TEST CRYSTAL-INDUCED ARTHRITIS GROUND PEPPER HYALURONATE MUCIN OCHRONOTIC SHARDS RHEUMATOID ARTHRITIS (RA) RHEUMATOID FACTOR (RF) RICE BODIES ROPE’S TEST SEPTIC ARTHRITIS Learning Objectives SYNOVIAL SYSTEMIC LUPUS ERYTHEMATOSUS 1. Define synovial. VISCOSITY 2. Describe the formation and function of synovial fluid. 3. Explain the collection and handling of synovial fluid. 4. Describe the appearance of normal and abnormal synovial fluids. 5. Correlate the appearance of synovial fluid with possible cause. 6. Interpret laboratory tests on synovial fluid. 7. Suggest further testing for synovial fluid, based on preliminary results. 8. List the four classes or categories of joint disease. 9. Correlate synovial fluid analyses with their representative disease classification. 253 LWBK461-c11_p253-262.qxd 11/18/09 6:04 PM Page 254 Aptara Inc 254 Graff’s Textbook of Routine Urinalysis and Body Fluids oint fluid is called synovial fluid because of its resem- blance to egg white. It is a viscous, mucinous substance Jthat lubricates most joints. Analysis of synovial fluid is important in the diagnosis of joint disease. Aspiration of joint fluid is indicated for any patient with a joint effusion or inflamed joints. Aspiration of asymptomatic joints is beneficial for patients with gout and pseudogout as these fluids may still contain crystals.1 Evaluation of physical, chemical, and microscopic characteristics of synovial fluid comprise routine analysis. This chapter includes an overview of the composition and function of synovial fluid, and laboratory procedures and their interpretations.
    [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]
  • 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]
  • Immune-Pathophysiology and -Therapy of Childhood Purpura
    Egypt J Pediatr Allergy Immunol 2009;7(1):3-13. Review article Immune-pathophysiology and -therapy of childhood purpura Safinaz A Elhabashy Professor of Pediatrics, Ain Shams University, Cairo Childhood purpura - Overview vasculitic disorders present with palpable Purpura (from the Latin, purpura, meaning purpura2. Purpura may be secondary to "purple") is the appearance of red or purple thrombocytopenia, platelet dysfunction, discolorations on the skin that do not blanch on coagulation factor deficiency or vascular defect as applying pressure. They are caused by bleeding shown in table 1. underneath the skin. Purpura measure 0.3-1cm, A thorough history (Table 2) and a careful while petechiae measure less than 3mm and physical examination (Table 3) are critical first ecchymoses greater than 1cm1. The integrity of steps in the evaluation of children with purpura3. the vascular system depends on three interacting When the history and physical examination elements: platelets, plasma coagulation factors suggest the presence of a bleeding disorder, and blood vessels. All three elements are required laboratory screening studies may include a for proper hemostasis, but the pattern of bleeding complete blood count, peripheral blood smear, depends to some extent on the specific defect. In prothrombin time (PT) and activated partial general, platelet disorders manifest petechiae, thromboplastin time (aPTT). With few exceptions, mucosal bleeding (wet purpura) or, rarely, central these studies should identify most hemostatic nervous system bleeding;
    [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]
  • T Helper Cell Infiltration in Osteoarthritis-Related Knee Pain
    Journal of Clinical Medicine Article T Helper Cell Infiltration in Osteoarthritis-Related Knee Pain and Disability 1, 1, 1 1 Timo Albert Nees y , Nils Rosshirt y , Jiji Alexander Zhang , Hadrian Platzer , Reza Sorbi 1, Elena Tripel 1, Tobias Reiner 1, Tilman Walker 1, Marcus Schiltenwolf 1 , 2 2 1, 1, , Hanns-Martin Lorenz , Theresa Tretter , Babak Moradi z and Sébastien Hagmann * z 1 Clinic for Orthopedics and Trauma Surgery, Center for Orthopedics, Trauma Surgery and Spinal Cord Injury, Heidelberg University Hospital, Schlierbacher Landstr. 200a, 69118 Heidelberg, Germany; [email protected] (T.A.N.); [email protected] (N.R.); [email protected] (J.A.Z.); [email protected] (H.P.); [email protected] (R.S.); [email protected] (E.T.); [email protected] (T.R.); [email protected] (T.W.); [email protected] (M.S.); [email protected] (B.M.) 2 Department of Internal Medicine V, Division of Rheumatology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany; [email protected] (H.-M.L.); [email protected] (T.T.) * Correspondence: [email protected]; Tel.: +49-622-1562-6289; Fax: +49-622-1562-6348 These authors contributed equally to this study. y These authors share senior authorship. z Received: 16 June 2020; Accepted: 23 July 2020; Published: 29 July 2020 Abstract: Despite the growing body of literature demonstrating a crucial role of T helper cell (Th) responses in the pathogenesis of osteoarthritis (OA), only few clinical studies have assessed interactions between Th cells and OA—related symptoms.
    [Show full text]