Changed Character of Osteomyelitis Memory Impairment Seemed Related to the Deficiency in Dr
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Imaging of Osteomyelitis: the Key Is in the Combination
Special RepoRt Special RepoRt Imaging of osteomyelitis: the key is in the combination An accurate diagnosis of osteomyelitis requires the combination of anatomical and functional imaging techniques. Conventional radiography is the first imaging modality to begin with, as it provides an overview of both the anatomy and the pathologic conditions of the bone. Sonography is most useful in the diagnosis of fluid collections, periosteal involvement and soft tissue abnormalities, and may provide guidance for diagnostic or therapeutic interventions. MRI highlights sites with tissue edema and increased regional perfusion, and provides accurate information of the extent of the infectious process and the tissues involved. To detect osteomyelitis before anatomical changes are present, functional imaging could have some advantages over anatomical imaging. Fluorine-18 fluorodeoxyglucose-PET has the highest diagnostic accuracy for confirming or excluding the diagnosis of chronic osteomyelitis. For both SPECT and PET, specificity improves considerably when the scintigraphic images are fused with computed tomography. Close cooperation between clinicians and imagers remains the key to early and adequate diagnosis when osteomyelitis is suspected or evaluated. †1 KEYWORDS: computed tomography n hybrid systems n imaging n MRI n nuclear Carlos Pineda , medicine n osteomyelitis n ultrasonography Angelica Pena2, Rolando Espinosa2 & Cristina Osteomyelitis is inflammation of the bone that osteomyelitis. The ideal imaging technique Hernández-Díaz1 is usually due to infection. There are different should have a high sensitivity and specificity; 1Musculoskeletal Ultrasound Department, Instituto Nacional de classification systems to categorize osteomyeli- numerous studies have been published con- Rehabilitacion, Avenida tis. Traditionally, it has been labeled as acute, cerning the accuracy of the various modali- Mexico‑Xochimilco No. -
A Comparison of Imaging Modalities for the Diagnosis of Osteomyelitis
A comparison of imaging modalities for the diagnosis of osteomyelitis Brandon J. Smith1, Grant S. Buchanan2, Franklin D. Shuler2 Author Affiliations: 1. Joan C Edwards School of Medicine, Marshall University, Huntington, West Virginia 2. Marshall University The authors have no financial disclosures to declare and no conflicts of interest to report. Corresponding Author: Brandon J. Smith Marshall University Joan C. Edwards School of Medicine Huntington, West Virginia Email: [email protected] Abstract Osteomyelitis is an increasingly common pathology that often poses a diagnostic challenge to clinicians. Accurate and timely diagnosis is critical to preventing complications that can result in the loss of life or limb. In addition to history, physical exam, and laboratory studies, diagnostic imaging plays an essential role in the diagnostic process. This narrative review article discusses various imaging modalities employed to diagnose osteomyelitis: plain films, computed tomography (CT), magnetic resonance imaging (MRI), ultrasound, bone scintigraphy, and positron emission tomography (PET). Articles were obtained from PubMed and screened for relevance to the topic of diagnostic imaging for osteomyelitis. The authors conclude that plain films are an appropriate first step, as they may reveal osteolytic changes and can help rule out alternative pathology. MRI is often the most appropriate second study, as it is highly sensitive and can detect bone marrow changes within days of an infection. Other studies such as CT, ultrasound, and bone scintigraphy may be useful in patients who cannot undergo MRI. CT is useful for identifying necrotic bone in chronic infections. Ultrasound may be useful in children or those with sickle-cell disease. Bone scintigraphy is particularly useful for vertebral osteomyelitis. -
Hypophosphatasia: Current Literature for Pathophysiology, Clinical Manifestations, Diagnosis, and Treatment
Open Access Review Article DOI: 10.7759/cureus.8594 Hypophosphatasia: Current Literature for Pathophysiology, Clinical Manifestations, Diagnosis, and Treatment Abdulai Bangura 1 , Lisa Wright 2 , Thomas Shuler 2 1. Department of Research, Trinity School of Medicine, Ratho Mill, VCT 2. Department of Orthopaedics, Carilion Clinic, Roanoke, USA Corresponding author: Abdulai Bangura, [email protected] Abstract Hypophosphatasia (HPP) is a rare inherited bone disorder identified by impaired bone mineralization. There are seven subtypes of HPP mainly characterized by their age of onset. These subtypes consist of perinatal (prenatal) benign, perinatal lethal, infantile, childhood, adult, odontohypophosphatasia, and pseudohypophosphatasia. Due to limited awareness of the condition, either misdiagnosis or delayed diagnosis is common. Furthermore, the condition is frequently treated with contraindicated drugs. This literature illustrates the most recent findings on the etiology, pathophysiology, clinical manifestations, diagnosing, and treatment for HPP and its subtypes. The etiology of the disease consists of loss-of-function mutations of the ALPL gene on chromosome one, which encodes for tissue nonspecific isoenzyme of alkaline phosphatase (TNAP). A decrease of TNAP reduces inorganic phosphate (Pi) for bone mineralization and allows for an increase in inorganic pyrophosphate (PPi) and phosphorylated osteopontin (p-OPN), which further reduces bone mineralization. The combination of these processes softens bone and mediates a clinical presentation similar to rickets/osteomalacia. HPP has an additional wide range of clinical features depending on its subtype. Although a concrete diagnostic guideline has not yet been established, many studies have supported a similar method of identifying HPP. Clinical features, radiological findings, and/or biomarker levels of the disorder should raise suspicion and encourage the inclusion of HPP as a differential diagnosis. -
Osteomalacia and Osteoporosis D
Postgrad. med.J. (August 1968) 44, 621-625. Postgrad Med J: first published as 10.1136/pgmj.44.514.621 on 1 August 1968. Downloaded from Osteomalacia and osteoporosis D. B. MORGAN Department of Clinical Investigation, University ofLeeds OSTEOMALACIA and osteoporosis are still some- in osteomalacia is an increase in the alkaline times confused because both diseases lead to a phosphatase activity in the blood (SAP); there deficiency of calcium which can be detected on may also be a low serum phosphorus or a low radiographs of the skeleton. serum calcium. This lack of calcium is the only feature Our experience with the biopsy of bone is that common to the two diseases which are in all a large excess of uncalcified bone tissue (osteoid), other ways easily distinguishable. which is the classic histological feature of osteo- malacia, is only found in patients with the other Osteomalacia typical features of the disease, in particular the Osteomalacia will be discussed first, because it clinical ones (Morgan et al., 1967a). Whether or is a clearly defined disease which can be cured. not more subtle histological techniques will detect Osteomalacia is the result of an imbalance be- earlier stages of the disease remains to be seen. tween the supply of and the demand for vitamin Bone pains, muscle weakness, Looser's zones, D. The the following description of disease is raised SAP and low serum phosphate are the Protected by copyright. based on our experience of twenty-two patients most reliable aids to the diagnosis of osteomalacia, with osteomalacia after gastrectomy; there is no and approximately in that order. -
Immunopathologic Studies in Relapsing Polychondritis
Immunopathologic Studies in Relapsing Polychondritis Jerome H. Herman, Marie V. Dennis J Clin Invest. 1973;52(3):549-558. https://doi.org/10.1172/JCI107215. Research Article Serial studies have been performed on three patients with relapsing polychondritis in an attempt to define a potential immunopathologic role for degradation constituents of cartilage in the causation and/or perpetuation of the inflammation observed. Crude proteoglycan preparations derived by disruptive and differential centrifugation techniques from human costal cartilage, intact chondrocytes grown as monolayers, their homogenates and products of synthesis provided antigenic material for investigation. Circulating antibody to such antigens could not be detected by immunodiffusion, hemagglutination, immunofluorescence or complement mediated chondrocyte cytotoxicity as assessed by 51Cr release. Similarly, radiolabeled incorporation studies attempting to detect de novo synthesis of such antibody by circulating peripheral blood lymphocytes as assessed by radioimmunodiffusion, immune absorption to neuraminidase treated and untreated chondrocytes and immune coprecipitation were negative. Delayed hypersensitivity to cartilage constituents was studied by peripheral lymphocyte transformation employing [3H]thymidine incorporation and the release of macrophage aggregation factor. Positive results were obtained which correlated with periods of overt disease activity. Similar results were observed in patients with classical rheumatoid arthritis manifesting destructive articular changes. This study suggests that cartilage antigenic components may facilitate perpetuation of cartilage inflammation by cellular immune mechanisms. Find the latest version: https://jci.me/107215/pdf Immunopathologic Studies in Relapsing Polychondritis JERoME H. HERmAN and MARIE V. DENNIS From the Division of Immunology, Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio 45229 A B S T R A C T Serial studies have been performed on as hematologic and serologic disturbances. -
A Case of Osteitis Fibrosa Cystica (Osteomalacia?) with Evidence of Hyperactivity of the Para-Thyroid Bodies
A CASE OF OSTEITIS FIBROSA CYSTICA (OSTEOMALACIA?) WITH EVIDENCE OF HYPERACTIVITY OF THE PARA-THYROID BODIES. METABOLIC STUDY II Walter Bauer, … , Fuller Albright, Joseph C. Aub J Clin Invest. 1930;8(2):229-248. https://doi.org/10.1172/JCI100262. Research Article Find the latest version: https://jci.me/100262/pdf A CASE OF OSTEITIS FIBROSA CYSTICA (OSTEOMALACIA?) WITH EVIDENCE OF HYPERACTIVITY OF THE PARA- THYROID BODIES. METABOLIC STUDY IIF By WALTER BAUER,2 FULLER ALBRIGHT3 AND JOSEPH C. AUB (From the Medical Clinic of the Massachutsetts General Hospital, Boston) (Received for publication February 5, 1929) INTRODUCTION In a previous paper (1) we have pointed out certain characteristic responses in the calcium and phosphorus metabolisms resulting from parathormone4 administration to essentially normal individuals. In the present paper, similar studies will be reported on a patient who presented a condition suggestive of idiopathic hyperparathyroidism. CASE HISTORY The patient, Mr. C. M., sea captain, aged 30, was transferred from the Bellevue Hospital Service to the Special Study Ward of the Massachusetts General Hospital through the courtesy of Dr. Eugene F. DuBois, for further investigation of his calcium metabolism and for consideration of parathyroidectomy. His complete case history has been reported by Hannon, Shorr, McClellan and DuBois (2). It describes a man invalided for over three years with symptoms resulting from a generalized skeletal decalcification. (See x-rays, figs. 1 to 4.) 1 This is No. VII of the series entitled "Studies of Calcium and Phosphorus Metabolism" from the Medical Clinic of the Massachusetts General Hospital. 2 Resident Physician, Massachusetts General Hospital. ' Research Fellow, Massachusetts General Hospital and Harvard Medical School. -
A Case of Acute Osteomyelitis: an Update on Diagnosis and Treatment
International Journal of Environmental Research and Public Health Review A Case of Acute Osteomyelitis: An Update on Diagnosis and Treatment Elena Chiappini 1,*, Greta Mastrangelo 1 and Simone Lazzeri 2 1 Infectious Disease Unit, Meyer University Hospital, University of Florence, Florence 50100, Italy; [email protected] 2 Orthopedics and Traumatology, Meyer University Hospital, Florence 50100, Italy; [email protected] * Correspondence: elena.chiappini@unifi.it; Tel.: +39-055-566-2830 Academic Editor: Karin Nielsen-Saines Received: 25 February 2016; Accepted: 23 May 2016; Published: 27 May 2016 Abstract: Osteomyelitis in children is a serious disease in children requiring early diagnosis and treatment to minimize the risk of sequelae. Therefore, it is of primary importance to recognize the signs and symptoms at the onset and to properly use the available diagnostic tools. It is important to maintain a high index of suspicion and be aware of the evolving epidemiology and of the emergence of antibiotic resistant and aggressive strains requiring careful monitoring and targeted therapy. Hereby we present an instructive case and review the literature data on diagnosis and treatment. Keywords: acute hematogenous osteomyelitis; children; bone infection; infection biomarkers; osteomyelitis treatment 1. Case Presentation A previously healthy 18-month-old boy presented at the emergency department with left hip pain and a limp following a minor trauma. His mother reported that he had presented fever for three days, cough and rhinitis about 15 days before the trauma, and had been treated with ibuprofen for 7 days (10 mg/kg dose every 8 h, orally) by his physician. The child presented with a limited and painful range of motion of the left hip and could not bear weight on that side. -
An Unusual Cause of Back Pain in Osteoporosis: Lessons from a Spinal Lesion
Ann Rheum Dis 1999;58:327–331 327 MASTERCLASS Series editor: John Axford Ann Rheum Dis: first published as 10.1136/ard.58.6.327 on 1 June 1999. Downloaded from An unusual cause of back pain in osteoporosis: lessons from a spinal lesion S Venkatachalam, Elaine Dennison, Madeleine Sampson, Peter Hockey, MIDCawley, Cyrus Cooper Case report A 77 year old woman was admitted with a three month history of worsening back pain, malaise, and anorexia. On direct questioning, she reported that she had suVered from back pain for four years. The thoracolumbar radiograph four years earlier showed T6/7 vertebral collapse, mild scoliosis, and degenerative change of the lumbar spine (fig 1); but other investigations at that time including the eryth- rocyte sedimentation rate (ESR) and protein electophoresis were normal. Bone mineral density then was 0.914 g/cm2 (T score = −2.4) at the lumbar spine, 0.776 g/cm2 (T score = −1.8) at the right femoral neck and 0.738 g/cm2 (T score = −1.7) at the left femoral neck. She was given cyclical etidronate after this vertebral collapse as she had suVered a previous fragility fracture of the left wrist. On admission, she was afebrile, but general examination was remarkable for pallor, dental http://ard.bmj.com/ caries, and cellulitis of the left leg. A pansysto- lic murmur was heard at the cardiac apex on auscultation; there were no other signs of bac- terial endocarditis. She had kyphoscoliosis and there was diVuse tenderness of the thoraco- lumbar spine. Her neurological examination was unremarkable. on September 29, 2021 by guest. -
Adult Osteomalacia a Treatable Cause of “Fear of Falling” Gait
VIDEO NEUROIMAGES Adult osteomalacia A treatable cause of “fear of falling” gait Figure Severe osteopenia The left hand x-ray suggested the diagnosis of osteomalacia because of the diffuse demineralization. A 65-year-old man was hospitalized with a gait disorder, obliging him to shuffle laterally1 (video on the Neurology® Web site at www.neurology.org) because of pain and proximal limb weakness. He had a gastrectomy for cancer 7 years previously, with severe vitamin D deficiency; parathormone and alkaline phosphatase were increased, with reduced serum and urine calcium and phosphate. There was reduced bone density (figure). He was mildly hypothyroid and pancytopenic. B12 and folate levels were normal. Investigation for an endocrine neoplasm (CT scan, Octreoscan) was negative. EMG of proximal muscles was typical for chronic myopathy; nerve conduction studies had normal results. After 80 days’ supplementation with calcium, vitamin D, and levothyroxine, the patient walked properly without assistance (video); pancytopenia and alkaline phosphatase improved. Supplemental data at This unusual but reversible gait disorder may have resulted from bone pain and muscular weakness related to www.neurology.org osteomalacia2 and secondary hyperparathyroidism, with a psychogenic overlay. Paolo Ripellino, MD, Emanuela Terazzi, MD, Enrica Bersano, MD, Roberto Cantello, MD, PhD From the Department of Neurology, University of Turin (P.R.), and Department of Neurology, University of Eastern Piedmont (E.T., E.B., R.C.), AOU Maggiore della Carità, Novara, Italy. Author contributions: Dr. Ripellino: acquisition of data, video included; analysis and interpretation of data; writing and editing of the manuscript and of the video. Dr. Terazzi: analysis and interpretation of data. -
Tuberculosis – the Masquerader of Bone Lesions in Children MN Rasool FCS(Orth) Department of Orthopaedics, University of Kwazulu-Natal
SAOJ Autumn 2009.qxd 2/27/09 11:11 AM Page 21 CLINICAL ARTICLE SA ORTHOPAEDIC JOURNAL Autumn 2009 / Page 21 C LINICAL A RTICLE Tuberculosis – the masquerader of bone lesions in children MN Rasool FCS(Orth) Department of Orthopaedics, University of KwaZulu-Natal Reprint requests: Dr MN Rasool Department of Orthopaedics University of KwaZulu-Natal Private Bag 7 Congella 4001 Tel: (031) 260 4297 Fax: (031) 260 4518 Email: [email protected] Abstract Fifty-three children with histologically confirmed tuberculous osteomyelitis were treated between 1989 and 2007. The age ranged from 1–12 years. There were 65 osseous lesions (excluding spinal and synovial). Seven had mul- tifocal bone involvement. Four basic types of lesions were seen: cystic (n=46), infiltrative (n=7), focal erosions (n=6) and spina ventosa (n=7). The majority of lesions were in the metaphyses (n=36); the remainder were in the diaphysis, epiphysis, short tubular bones, flat bones and small round bones. Bone lesions resembled chronic infections, simple and aneurysmal bone cysts, cartilaginous tumours, osteoid osteoma, haematological bone lesions and certain osteochondroses seen during the same period of study. Histological confirmation is man- datory to confirm the diagnosis of tuberculosis as several bone lesions can mimic tuberculous osteomyelitis. Introduction The variable radiological appearance of isolated bone Tuberculous osteomyelitis is less common than skeletal lesions in children can resemble various bone lesions tuberculosis involving the spine and joints. The destruc- including subacute and chronic osteomyelitis, simple and tive bone lesions of tuberculosis, the disseminated and the aneurysmal bone cysts, cartilaginous tumours, osteoid multifocal forms, are less common now than they were 50 osteoma, granulomatous lesions, haematological disease, 6,7,12 years ago.1-7 However, in recent series, solitary involve- and certain malignant tumours. -
1019 2 Feb 11 Weisbrode FINAL.Pages
The Armed Forces Institute of Pathology Department of Veterinary Pathology Wednesday Slide Conference 2010-2011 Conference 19 2 February 2011 Conference Moderator: Steven E. Weisbrode, DVM, PhD, Diplomate ACVP CASE I: 2173 (AFIP 2790938). Signalment: 3.5-month-old, male intact, Chow-Rottweiler cross, canine (Canis familiaris). History: This 3.5-month-old male Chow-Rottweiler mixed breed dog was presented to a veterinary clinic with severe neck pain. No cervical vertebral lesions were seen radiographically. The dog responded to symptomatic treatment. A week later the dog again presented with neck pain and sternal recumbency. The nose was swollen, and the submandibular and popliteal lymph nodes were moderately enlarged. The body temperature was normal. A complete blood count (CBC) revealed a marked lymphocytosis (23,800 lymphocytes/uI). Over a 3-4 hour period there was a noticeable increase in the size of all peripheral lymph nodes. Treatment included systemic antibiotics and corticosteroids. The dog became ataxic and developed partial paralysis. The neurologic signs waxed and waned over a period of 7 days, and the lymphadenopathy persisted. The peripheral blood lymphocyte count 5 days after the first CBC was done revealed a lymphocyte count of 6,000 lymphocytes/uI. The clinical signs became progressively worse, and the dog was euthanized two weeks after the initial presentation. Laboratory Results: Immunohistochemical (IHC) staining of bone marrow and lymph node sections revealed that tumor cells were negative for CD3 and CD79α. Gross Pathology: Marked generalized lymph node enlargement was found. Cut surfaces of the nodes bulged out and had a white homogeneous appearance. The spleen was enlarged and meaty. -
Michael P. Whyte, M.D
Melorheostosis Michael P. Whyte, M.D. Center for Metabolic Bone Disease and Molecular Research, Shriners Hospital for Children; and Division of Bone and Mineral Diseases, Washington University School of Medicine at Barnes-Jewish Hospital; St. Louis, Missouri, U.S.A. 1 History • 1922 – Léri and Joanny (define the disorder) • “Léri’s disease” • 5000 BC (Chilean burial site 2-year-old girl) • 1500-year-old skeleton in Alaska 2 Definitions (Greek) melo=“limb” rhein=“to flow” osteon=“bone” • Melorheostosis means "limb and I(me)-Flow“ • Flowing Periosteal Hyperostosis • Candle guttering (dripping wax) on x-ray in adults • OMIM (Online Mendelian Inheritance of Man) % 155950 DISORDERS THAT CAUSE OSTEOSCLEROSIS Dysplasias Craniodiaphyseal dysplasia Osteoectasia with hyperphosphatasia Craniometaphyseal dysplasia Mixed sclerosing bone dystrophy Dysosteosclerosis Oculodento-osseous dysplasia Endosteal hyperostosis Osteodysplasia of Melnick and Needles Van Buchem Disease Osteoectasia with hyperphosphatasia Sclerosteosis (hyperostosis corticalis) Frontometaphyseal dysplasia Osteopathia striata Infantile cortical hyperostosis Osteopetrosis (Caffey disease) Osteopoikilosis Melorheostosis Progressive diaphyseal dysplasia Metaphyseal dysplasia (Pyle disease) (Engelmann disease) Pyknodysostosis Metabolic Carbonic anhydrase II deficiency Hyper-, hypo- and pseudohypoparathyroidism Fluorosis Hypophosphatemic osteomalacia Heavy metal poisoning Milk-alkali syndrome Hypervitaminosis A,D Renal osteodystrophy Other Axial osteomalacia Multiple myeloma Paget’s disease