RADIOLOGY

REVIEW
CMCC
Erin Ogrady

REFERENCES This information was complied from lecture notes, and Essentials of Skeletal Radiology (Yochum & Rowe).

Table of Contents
Intro to Cervical Spine & Some Basics ................................................................................... 9 Canadian C-Spine Rules ............................................................................................................ 9 Introduction to Thoracic Spine ................................................................................................. 9 Introduction to Lumbar Spine ............................................................................................... 10 Introduction to Pelvis ............................................................................................................... 11 Introduction to the Knee ......................................................................................................... 11 Ottawa Knee Rules ................................................................................................................... 12 Introduction to the Ankle & Foot ...................................................................................... 12 Ottawa Ankle Rules ................................................................................................................. 13 Introduction to the Shoulder ................................................................................................. 13 Introduction to the Elbow ....................................................................................................... 14 Introduction to the Wrist ........................................................................................................ 14 Indications to X-Ray Kids for back pain .............................................................................. 15 The Pediatric Spine .................................................................................................................... 15 The Skull ........................................................................................................................................ 15

ROENTGENOMETRICS .......................................................................... 15 Cervical Spine Roentgenometrics ......................................................................................... 15 Thoracic Spine Roentgenometrics ....................................................................................... 16 Lumbar Spine Roentgenometrics ......................................................................................... 16 Foot Roentgenometrics ......................................................................................................... 17 Sacral Spine Roentgenometrics ............................................................................................ 17 Pelvic Roentgenometrics ......................................................................................................... 17 Shoulder Roentgenometrics .................................................................................................. 17 Elbow Roentgenometrics ........................................................................................................ 17 Wrist Roentgenometrics .......................................................................................................... 17 Pediatric Pelvis Roentgenometrics ...................................................................................... 17 IMAGING MODALITIES ......................................................................... 18 Bone Scans (Scintography) ..................................................................................................... 18 DEXA (Dual Energy X-ray Absorptiometry) ....................................................................... 18 CT (Computed Tomography) .................................................................................................. 18 MRI .................................................................................................................................................. 18 SKELETAL ANOMALIES ......................................................................... 19 Dens Anomalies and Fractures .............................................................................................. 19

Congenital Block Vertebra ...................................................................................................... 19 Acquired Block Vertebrae ....................................................................................................... 19 Klippel-Feil Syndrome .............................................................................................................. 19 Omovertebral Bone .................................................................................................................. 19 Sprengels Deformity ................................................................................................................ 20 Posterior Ponticle/Pons Ponticus ......................................................................................... 20 Paramastoid/Epitransverse Process ................................................................................... 20 Spina Bifida Occulta/Schisis Defect/Cleft Spinous ......................................................... 20 No Name Anomaly .................................................................................................................... 20 Calcification of the Stylo-Hyoid Ligament ......................................................................... 20 Unfused Secondary Ossification Centers for Spinous Processes .............................. 20 Pedicle Agenesis ........................................................................................................................ 20 Facet Tropism ............................................................................................................................. 20 Butterfly Vertebrae ................................................................................................................... 20 Hemivertebra (HV) .................................................................................................................... 21 Spondylolisthesis ....................................................................................................................... 21 Scheuermanns Disease ........................................................................................................... 21 Hahns Clefts ............................................................................................................................... 21 Notochordal Remnants/Nuclear Impressions ................................................................. 21 Schmorls Node .......................................................................................................................... 22 Limbus Bone ................................................................................................................................ 22 Knife Clasp Deformity .............................................................................................................. 22 Transitional Vertebrae ............................................................................................................. 22 Spatulated TVPs ........................................................................................................................ 22 Congenital Absence of Pedicle (AKA Pedicle Agenesis) ................................................ 22 Para-Auricular Sulci/Para Glenoid Sulci ............................................................................. 22 Supracondylar Process .......................................................................................................... 22 Coronoid Bone & Os Supratrochlear Dorsale (Joint Mice) ................................. 22 Slipped Capital Femoral Epiphysis (SCFE) ................................................................... 22 Developmental Dysplasia of the Hip (DDH) ................................................................. 22 Os Acetabulae ............................................................................................................................ 23 Bipartite Patella ....................................................................................................................... 23 Dorsal Defect of the Patella ................................................................................................. 23 Tarsal Coalition ........................................................................................................................ 23 Persistent Synchondrosis .................................................................................................... 23 Talar Beak ................................................................................................................................... 24 Os Trigonum .............................................................................................................................. 24 Os Trigonum Syndrome ........................................................................................................ 24 Os Intermetatarseum ............................................................................................................. 24 Other Os Bones ......................................................................................................................... 24

RADIOLOGY REVIEW

Os Acromiale .............................................................................................................................. 24 Supracondylar Process (Humerus) .................................................................................. 24 Coronoid Bone and Os Supratrochleare Dorsale ........................................................ 24 Bilateral Madelungs Deformity ......................................................................................... 24 Terry Thomas Sign .................................................................................................................. 24 Negative Ulnar Variance ....................................................................................................... 24 Positive Ulnar Variance ......................................................................................................... 24 Os Syloideum ............................................................................................................................. 24 The Normal Apophysis of the 5th Metatarsal ............................................................... 24 Bipartite Sesamoids ................................................................................................................ 24 Club Foot ...................................................................................................................................... 24 Anomalous Feet ........................................................................................................................ 24 Polydactyly ................................................................................................................................. 25 Osteopoikilosis .......................................................................................................................... 25

CONDITIONS ........................................................................................ 25 Scoliosis ......................................................................................................................................... 25 Achondroplasia ........................................................................................................................... 25 Osteogenesis Imperfecta ........................................................................................................ 25 Osteopetrosis .............................................................................................................................. 26 Osteopoikilosis ............................................................................................................................ 26 Neurofibromatosis ..................................................................................................................... 26 Pressure Erosions ....................................................................................................................... 27 Marfans Syndrome ................................................................................................................... 27 Cleidocranial Dysostosis (Dysplasia) .................................................................................... 27 Downs Syndrome/Trisomy 21 .............................................................................................. 27 Osteoporosis (OP) ...................................................................................................................... 28 Osteopenia (Op) ......................................................................................................................... 28 Osteomalacia (OM) ................................................................................................................... 28 Hyperparathyroidism (HPTH) ................................................................................................. 29 Cushings Syndrome .................................................................................................................. 29 Acromegaly .................................................................................................................................. 29 BONE TUMORS .................................................................................... 29 Benign Osseous Lesions ........................................................................................................... 31 Osteochondroma ....................................................................................................................... 31 Hereditary Multiple Exostosis (HME) ................................................................................ 31 Enostoma/Bone Island ............................................................................................................ 31 Osteoid Osteoma (OO) ............................................................................................................ 31 Osteoblastoma/Osteoid Blastoma ..................................................................................... 32

Benign Cartilaginous Lesions ................................................................................................. 32 Enchondroma ............................................................................................................................. 32 Olliers Disease (Multiple Enchondromatosis) ............................................................... 32 Maffuccis Syndrome ............................................................................................................... 32 Chondroblastoma (Codmans Tumor) .............................................................................. 32 Benign Fibrous Lesions ............................................................................................................ 32 Fibrous Xanthoma (Non-Ossifying Fibromas & Fibrous Cortical Defects) ......... 33 Fibrous Dysplasia (FD) ............................................................................................................. 33 McCune Albright Syndrome .................................................................................................. 33 Benign Cystic Bone Lesions .................................................................................................... 33 Simple Bone Cyst (SBC) ........................................................................................................... 33 Aneurysmal Bone Cyst (ABC) ................................................................................................ 33 Miscellaneous Benign Bone Tumors ................................................................................... 34 Intraosseous Lipoma ................................................................................................................ 34 Hemangioma .............................................................................................................................. 34 Osteoma ....................................................................................................................................... 34 Primary Quasi-Malignant Bone Tumors ............................................................................ 34 Giant Cell Tumor (GCT) ........................................................................................................... 34 Osseous Malignant Bone Tumors ........................................................................................ 35 Osteosarcoma ............................................................................................................................ 35 Parosteal Osteosarcoma ........................................................................................................ 35 Cartilaginous Malignant Bone Tumors ............................................................................... 35 Chondrosarcoma ....................................................................................................................... 35 Fibrous Malignant Bone Tumors .......................................................................................... 36 Fibrosarcoma .............................................................................................................................. 36 Round Cell Malignant Bone Tumors ................................................................................... 36 Solitary Plasmacytoma ........................................................................................................... 36 Multiple Myeloma (MM) ....................................................................................................... 36 Ewings Sarcoma ....................................................................................................................... 37 Hodgkins Lymphoma (HL) .................................................................................................... 37 Non-Hodgkins Lymphoma (NHL) ....................................................................................... 37 Synovial Sarcoma ...................................................................................................................... 37 Adamantinoma .......................................................................................................................... 37 Miscellaneous Tumors ............................................................................................................. 37 Chordoma .................................................................................................................................... 38 Bone Metastasis ......................................................................................................................... 38 Drop Metastasis ........................................................................................................................ 39 Lytic Metastasis ......................................................................................................................... 39

Blastic Metastasis ..................................................................................................................... 39 Mixed Metastasis ...................................................................................................................... 39 Blown-Out Metastasis ............................................................................................................. 39

BONE INFECTIONS ................................................................................ 39 PAGETS DISEASE (THE GREAT MIMIC) .............................................. 42 HEMATOLOGIC DISORDERS .................................................................. 43 Sickle Cell Anemia .................................................................................................................... 43 Thalassemia ................................................................................................................................ 43 Sickle Cell Dacylitis .................................................................................................................. 44 AVN of the Femoral Head ..................................................................................................... 44 Hemophilia .................................................................................................................................. 44 Leukemia ..................................................................................................................................... 44 Osteonecrosis ............................................................................................................................ 45 AVN (Hip and Spine) ............................................................................................................... 45 Metaphyseal/Diaphyseal AVN ............................................................................................ 45 Medullary Infarction ............................................................................................................... 45 Legg-Calve-Perthes Disease ................................................................................................ 45 Spontaneous Osteonecrosis of the Femoral Head ..................................................... 46 Caisson Disease ......................................................................................................................... 46 Freibergs Disease .................................................................................................................... 46 Keinbocks Disease .................................................................................................................. 46 Spontaneous Osteonecrosis of the Knee (SONK) ....................................................... 46 Osgood-Schlatters Disease .................................................................................................. 46 Osteochondritis Dessicans (OCD) ..................................................................................... 46 Blounts Disease ........................................................................................................................ 47 Diazs Disease ............................................................................................................................ 47 Hasss Disease ............................................................................................................................ 47 Kohlers Disease ........................................................................................................................ 47 Mauclaires Disease ................................................................................................................. 47 Panners Disease ....................................................................................................................... 47 Preisers Disease ....................................................................................................................... 47 Severs Disease .......................................................................................................................... 47 Singing-Larden-Johansson Disease .................................................................................. 47 Arterial Disorders ................................................................................ 47 Atherosclerosis ......................................................................................................................... 47 Monchkebergs Medial Sclerosis ....................................................................................... 47 Aneurysms .................................................................................................................................. 47 Venous Insufficiency ............................................................................................................... 48

Nutritional, Metabolic and Endocrine Diseases .................................... 48 Osteoporosis .............................................................................................................................. 48 Senile/Postmenopausal Osteoporosis ............................................................................. 48 Regional Osteoporosis ........................................................................................................... 48
Reflex Sympathetic Dystrophy Syndrome (AKA Complex Regional Pain Syndrome) ................................................................................................................................... 48 Disuse and Immobilization Osteoporosis ...................................................................... 48 Transient Regional Osteoporosis ...................................................................................... 48 Heavy Metal Poisoning .......................................................................................................... 48 Rickets .......................................................................................................................................... 49 Osteomalacia ............................................................................................................................. 49 Hyperparathyroidism ............................................................................................................ 49 Scurvy ........................................................................................................................................... 49 Acromegaly ................................................................................................................................ 49 Diabetes ....................................................................................................................................... 49

Trauma ................................................................................................ 49 Fractures & Dislocations ...................................................................................................... 50 Cervical Spine Trauma .......................................................................................................... 52 Thoracic and Lumbar Trauma .......................................................................................... 52 Sacral Trauma .......................................................................................................................... 53 Knee Trauma ............................................................................................................................. 53 Stress Fractures ........................................................................................................................ 53 Growth Plate Injuries/Salter-Harris-Epiphyseal Injuries ...................................... 53 Myositis Ossificans .................................................................................................................. 53 Jefferson Fracture (Burst Fracture of C1) ..................................................................... 53 Odontoid Fracture ................................................................................................................... 54 Hangmans Fracture ............................................................................................................... 54 Flexion-Type Teardrop Fracture ...................................................................................... 54 Post-Traumatic Cord Myelomalacia ................................................................................ 54 Unilateral Locked Facets ...................................................................................................... 54 Bilateral Locked Facets ......................................................................................................... 54 Pseudosubluxation .................................................................................................................. 54 Chance Fracture ....................................................................................................................... 54 Lumbar Ossified Bridge Syndrome (LOBS) .................................................................. 54 Traumatic Syringohydromyelia ........................................................................................ 54 Posterior Apophyseal Ring Fracture ............................................................................... 55 TVP Fractures ............................................................................................................................ 55 Sternal Fractures ..................................................................................................................... 55 Rib Fractures ............................................................................................................................. 55 Wedge Fractures ...................................................................................................................... 55

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Burst Fractures ......................................................................................................................... 55 Sacral Fractures ........................................................................................................................ 55 Malgaignes Fracture .............................................................................................................. 55 Bucket Handle Fracture ........................................................................................................ 55 Sprung Pelvis ............................................................................................................................. 55 Pubic Diastasis .......................................................................................................................... 55 Straddle Fracture ..................................................................................................................... 55 Coccyx Fracture ........................................................................................................................ 55 Iliac Wing Fracture .................................................................................................................. 56 Avulsion Fracture ..................................................................................................................... 56 Hip Trauma ................................................................................................................................. 56 Intracapsular Hip Fractures ................................................................................................ 56 Extracapsular Hip Fractures ............................................................................................... 56 Hip Dislocations ........................................................................................................................ 56 Posterior Hip Dislocation ..................................................................................................... 56 Anterior Hip Dislocation ....................................................................................................... 56 Central Hip Dislocation .......................................................................................................... 56 Supracondylar Fracture (Distal Femur) ......................................................................... 56 Femoral Condylar Fracture ................................................................................................. 57 Tibial Plateau (Bumper or Fender Fracture) ............................................................... 57 Trampoline Fracture .............................................................................................................. 57 Segonds Fracture .................................................................................................................... 57 Proximal Fibular Fracture .................................................................................................... 57 Patellar Fractures .................................................................................................................... 57 Patellar Dislocation ................................................................................................................. 57 Femorotibial Dislocation ...................................................................................................... 57 Proximal Tibiofibular Dislocation ..................................................................................... 57 Internal Derangement: Ligamentous Injuries ............................................................. 57 Osgood Schlatters ................................................................................................................... 57 Medial Malleolus Fracture .................................................................................................... 58 Lateral Malleolus Fracture ................................................................................................... 58 Bimalleolar Fracture ............................................................................................................... 58 Trimalleolar Fracture ............................................................................................................. 58 Potts Fracture ........................................................................................................................... 58 Dupuytrens Fracture ............................................................................................................. 58 Maisonneuves Fracture ........................................................................................................ 58 Tillauxs Fracture ..................................................................................................................... 58 Toddlers Fracture ................................................................................................................... 58 Talar Dislocations .................................................................................................................... 58 Calcaneus Fractures/Calcaneal Compression ............................................................. 58

Talus Fractures ......................................................................................................................... 59 Navicular Fracture .................................................................................................................. 59 Cuneiform Fracture ................................................................................................................ 59 Cuboid Fracture ........................................................................................................................ 59 Metatarsals Fracture, the Jones (Dancers) Fracture .............................................. 59 Phalangeal Fractures ............................................................................................................. 59 Crush Fracture .......................................................................................................................... 59 Bedroom Fracture ................................................................................................................... 59 Chip Fracture ............................................................................................................................. 59 Hallux Rigidus ........................................................................................................................... 59 Sesamoid Fractures ................................................................................................................ 59 Midtarsal Chopart's Dislocations .................................................................................. 59 Tarsometatarsal Lisfracs Dislocation ........................................................................ 59 Osteochondritis Dissecans .................................................................................................. 59 Labral Tears ............................................................................................................................... 59 Rotator Cuff Tears ................................................................................................................... 60 Tendinitis and Bursitis .......................................................................................................... 60 Fracture of the Clavicle ......................................................................................................... 60 Scapular Fracture and Bankart Lesions ......................................................................... 60 General Humeral Fractures (Flap and Hill Sachs Fractures) ................................ 60 Fractures of the Proximal Humerus ................................................................................ 60 Anterior Shoulder Dislocations ......................................................................................... 60 Posterior Shoulder Dislocations ....................................................................................... 60 Inferior Shoulder Dislocations ........................................................................................... 61 Superior Shoulder Dislocations ......................................................................................... 61 Acromioclavicular (AC) Joint Separations .................................................................... 61 Acro-Osteolysis of the Distal Clavicle ............................................................................. 61 Elbow and Forearm Trauma ............................................................................................... 61 Supracondylar Fractures of the Humerus .................................................................... 61 Intercondylar Fractures of the Humerus ...................................................................... 61 Condylar Fracture ................................................................................................................... 61 Epicondylar Fracture ............................................................................................................. 61 Olecranon Fracture in the Proximal Ulna ..................................................................... 61 Coronoid Fracture ................................................................................................................... 62 Radial Head Fractures and Chisel Fractures ................................................................ 62 Radial Neck Fractures ............................................................................................................ 62 Nightstick (Parry) Fracture ................................................................................................. 62 Monteggia Fracture ................................................................................................................ 62 Galeazzi Fracture ..................................................................................................................... 62 Elbow Dislocations ................................................................................................................. 62

Colles Fracture .......................................................................................................................... 62 Smiths (Reversed Colles) Fracture .................................................................................. 62 Bartons (Rim) Fracture ........................................................................................................ 62 Reverse Bartons Fracture ................................................................................................... 62 Radial Styloid/Chauffeaurs Fracture (Backfire, Hutchinsons Fracture) ....... 62 Fracture through the Distal Ulna/Nightstick Fracture ............................................ 62 Scaphoid Fracture .................................................................................................................... 62 Triquetrum Fracture .............................................................................................................. 62 Pisiform Fracture ..................................................................................................................... 63 Lunate Dislocation ................................................................................................................... 63 Scaphoid Dislocation .............................................................................................................. 63 Perilunate Dislocation ............................................................................................................ 63 Trans-Scaphoid Perilunate Dislocation .......................................................................... 63 Boxers Fracture ....................................................................................................................... 63 Bar-Room Fracture .................................................................................................................. 63 Metacarpal Shaft Fractures .................................................................................................. 63 Metacarpal Base Fractures .................................................................................................. 63 Bennetts Fracture/Skiers Fracture ................................................................................ 63 Rolando Fracture ..................................................................................................................... 63 Transverse Fracture through the 1st Metacarpal ....................................................... 63 Phalangeal Fracture ................................................................................................................ 63 Gamekeepers Thumb ............................................................................................................ 63 Interphalangeal Dislocation ................................................................................................ 63 Mallet Finger .............................................................................................................................. 63

Arthritides ........................................................................................... 64 Terminology and Background Information ................................................................. 64 Types of Joints ............................................................................................................................ 64 Patterns of Joint Involvement ............................................................................................. 64 Arthritides ................................................................................................................................... 65 Disc Lesions ................................................................................................................................ 65 Disc Bulge .................................................................................................................................... 65 Contained Central Disc Herniations ................................................................................. 65 Contained Paracentral Disc Herniations ....................................................................... 65 Contained Far Lateral Disc Herniations ........................................................................ 65 Non-Contained Sequestered Discs .................................................................................... 65 Inflammatory Arthritides Rheumatoid Factor Positive ....................................... 66 Chest Radiology ................................................................................... 75 Rheumatoid Arthritis (RA) ................................................................................................... 66 Imaging ........................................................................................................................................ 75 Juvenile Rheumatoid Arthritis/Juvenile Chronic Polyarthritis (JRA) ................ 66 X-Ray ............................................................................................................................................. 75 Protrusio Acetabuli ................................................................................................................. 67 CT Scan ......................................................................................................................................... 75 Osteolysis of the Distal Clavicle .......................................................................................... 67 Nuclear Scintigraphy ............................................................................................................. 76

Systemic Lupus Erythematosis (SLE) ............................................................................. 67 Scleroderma ............................................................................................................................... 67 Degenerative Arthritides ...................................................................................................... 67 Bunions ......................................................................................................................................... 68 Spinal Stenosis .......................................................................................................................... 68 Lateral Recess Entrapment ................................................................................................. 68 Cervical Spondylotic Myelopathy (CSM) ........................................................................ 68 OA of the Hands ........................................................................................................................ 68 GH Joint OA ................................................................................................................................. 68 AC Joint OA .................................................................................................................................. 69 Degenerative Disc Disease (DDD) ..................................................................................... 69 Degenerative Spondylolisthesis ......................................................................................... 69 Facet Arthrosis .......................................................................................................................... 69 Baastrups Disease .................................................................................................................. 69 Cervical Spine DDD/DJD ....................................................................................................... 69 DISH (Diffuse Ideopathic Skeletal Hyperplasia) ........................................................ 69 OPLL (Ossification of the Posterior Longitudinal Ligament) ............................... 70 Erosive OA ................................................................................................................................... 70 Seronegative Spondyloarthropaties ................................................................................ 70 AS (Ankylosing Spondylitis) ................................................................................................ 71 Sacroillitis ................................................................................................................................... 71 Enteropathic Arthritis (EA) ................................................................................................. 72 Psoriatic Arthritis .................................................................................................................... 72 Reactive Arthritis ..................................................................................................................... 72 Metabolic Arthropathies ...................................................................................................... 72 Gout ................................................................................................................................................ 72 CPPD (Calcium Pyrophosphate Dihydrate Crystal Deposition Disease) .......... 72 Miscellaneous Arthropathies ............................................................................................. 73 Neurotrophic Arthropathy .................................................................................................. 73 Syringomyelia ............................................................................................................................ 73 Hypertrophic Osteoarthropathy (HOA) ........................................................................ 73 Synoviochondrometaplasia ................................................................................................. 73 HADD (Hydroxyapatite Deposition Disease) ............................................................... 74 Diseases Associated with Chondrocalcinosis ............................................................... 74 Pnemonics for the Arthropathies ..................................................................................... 74

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Nuclear Perfusion Scans ........................................................................................................ 76 Pulmonary Arterial Angiogram ......................................................................................... 76 Evaluating Chest X-Rays ........................................................................................................ 76 Search Pattern for Upright PA ............................................................................................ 77 Search Pattern for the Lateral Chest View .................................................................... 77 The Apical Lordotic View Taken AP ................................................................................. 78 Lobar Anatomy .......................................................................................................................... 78 More Anatomy ........................................................................................................................... 78 Thoracic Anomalies ................................................................................................................. 78 SRBs Anomaly ........................................................................................................................... 78 Lushkas Bifurcated Rib ......................................................................................................... 78 Rib Foramen ............................................................................................................................... 78 Rib Fusion .................................................................................................................................... 78 Intrathoracic Rib ...................................................................................................................... 78 Pectus Excavatum .................................................................................................................... 78 Pectus Carinatum ..................................................................................................................... 78 Costochondral Calcification ................................................................................................ 79 Pulmonary Conditions and Findings ............................................................................... 79 Lobar Consolidation ................................................................................................................ 79 The Air Bronchogram Sign .................................................................................................. 79 Atelectasis/Collapsed Lung ................................................................................................. 79 Pleural Effusion ......................................................................................................................... 80 Pleural Calcification ............................................................................................................... 80 Extrapleural Sign ..................................................................................................................... 80 Meniscus Sign ............................................................................................................................. 80 Silhouette Sign ........................................................................................................................... 81 Plasmacytoma ........................................................................................................................... 81 Rib Fractures .............................................................................................................................. 81 Elevated Diaphragm ............................................................................................................... 81 Hilar Enlargement ................................................................................................................... 81 Mediastinal Enlargement ..................................................................................................... 81 Anterior Mediastinal Masses ............................................................................................... 82 Middle Mediastinal Mass ...................................................................................................... 82 Posterior Mediastinal Masses ............................................................................................. 82 Interstitial/Infiltrative Disease .......................................................................................... 82 Diffuse Interstitial Pattern ................................................................................................... 82 Solitary Nodules ........................................................................................................................ 82 Multiple Nodules ....................................................................................................................... 83 Cavitating Nodules .................................................................................................................. 83 Bronchogenic Cyst ................................................................................................................... 83

Hamartoma ................................................................................................................................ 83 Bronchogenic Carcinoma ..................................................................................................... 83 Adenocarcinoma ...................................................................................................................... 83 Squamous Cell Carcinoma ................................................................................................... 83 Small Cell Carcinoma ............................................................................................................. 83 Large Cell Carcinoma ............................................................................................................. 83 Pancoast Tumor ....................................................................................................................... 84 Metastasis ................................................................................................................................... 84 Cardiovascular Conditions and Findings ...................................................................... 84 Increased Cardiac Silhouette .............................................................................................. 84 Cardiomegaly ............................................................................................................................ 84 Thoracic Aortic Aneurysm ................................................................................................... 84 Inhalation Diseases ................................................................................................................. 84 Pneumoconiosis ........................................................................................................................ 84 Silicosis ......................................................................................................................................... 85 Asbestosis .................................................................................................................................... 85 Lime Dust Exposure ................................................................................................................ 85 Rheumatoid ................................................................................................................................ 85 Obstructive Lung Diseases .................................................................................................. 85 Asthma .......................................................................................................................................... 85 Bronchiectasis ........................................................................................................................... 85 COPD .............................................................................................................................................. 86 Emphysema ................................................................................................................................ 86 Bullous Emphysema ................................................................................................................ 86 Chronic Bronchitis/Bronchiolitis ...................................................................................... 86 Pneumonia .................................................................................................................................. 86 Acute/Typical Bacterial Pneumonia ............................................................................... 86 Atypical Viral Pneumonia .................................................................................................... 86 Lung Abscess .............................................................................................................................. 87 Pulmonary TB (and a bit about granulomatous diseases) .................................... 87 Pneumothorax .......................................................................................................................... 88 Nodules ........................................................................................................................................ 88 Calcified Granuloma ............................................................................................................... 88 Multiple Pulmonary Nodules .............................................................................................. 88 Pulmonary Metastasis ........................................................................................................... 89 Lymphoma .................................................................................................................................. 89 Histoplasmosis .......................................................................................................................... 89 Tuberculosis ............................................................................................................................... 89 Rheumatoid Nodules .............................................................................................................. 89 Wegeners Granulomatosis .................................................................................................. 89

Cardiovascular Imaging ........................................................................................................ 89 Pericarditis .................................................................................................................................. 89 Congestive Heart Failure (CHF) ......................................................................................... 90 Thoracic Aortic Aneurysm ................................................................................................... 90 Pulmonary Hypertension ...................................................................................................... 90 Hernias ......................................................................................................................................... 90 Review Comparisons .......................................................................................................... 91 Collapse vs. Consolidation .................................................................................................... 91 Pneumothorax vs. Tension Pneumothorax ................................................................... 91 Interstitial Pattern vs. Consolidation .............................................................................. 91 Diaphragm Elevation vs. Pleural Effusion .................................................................... 91 Chest Differentials ................................................................................................................... 91

Radiology Promises .............................................................................. 94 Imaging Techniques ................................................................................................................ 95 KUB recumbent view .............................................................................................................. 95 Barium studies ........................................................................................................................... 95 IVP ................................................................................................................................................... 96 Diagnostic Ultrasound ........................................................................................................... 96 CT .................................................................................................................................................... 96 MRI ................................................................................................................................................. 96 ABCs & Reading the FIlm ..................................................................................................... 96
Organ Enlargement/Displacement, Anomalies, & Abnormal Abdominal Air Patterns ........................................................................................................................................ 97 Hepatomegaly/Liver Enlargement .................................................................................. 97 Splenomegaly/Enlargement of the Spleen .................................................................... 98 Kidneys Conditions .................................................................................................................. 98 Kidney Enlargement ............................................................................................................... 99 Horseshoe Kidney ..................................................................................................................... 99 Pelvic Kidney .............................................................................................................................. 99 Malrotation of a Kidney ........................................................................................................ 99 Crossed Ectopy .......................................................................................................................... 99 Duplication of the Collecting System ............................................................................... 99 Obstruction of the Bladder ................................................................................................ 100 Large Bowel Conditions ..................................................................................................... 100 Toxic Megacolon .................................................................................................................... 100 LBO/Large Bowel Obstruction ........................................................................................ 100 Adynamic/Paralytic Ileus .................................................................................................. 100 Diverticulitis ............................................................................................................................ 100 Crohns Disease/Regional Enteritis ............................................................................... 100 Ascites ......................................................................................................................................... 101

Small Bowel .............................................................................................................................. 101 Abnormal Small Bowel Air ................................................................................................ 101 Adynamic or Paralytic Ileus .............................................................................................. 102 SBO/Small Bowel Obstruction ......................................................................................... 102 Gallstone Ileus ......................................................................................................................... 102 Gallbladder ............................................................................................................................... 102 Air in the Biliary Tree .......................................................................................................... 102 Emphysematous Cholecystitis .......................................................................................... 103 Ovaries ....................................................................................................................................... 103 Ovarian Carcinoma ............................................................................................................... 103 Pneumoperitoneum ............................................................................................................. 103 Colostomy Stoma ................................................................................................................... 103 Intra-Abdominal Calcifications and Other Interesting Densities ..................... 103 Concretions .............................................................................................................................. 104 Gallstones (Choleliths), Cholelithiasis (Concretions) ............................................. 104 Phleboliths ................................................................................................................................ 104 Fecolith/Appendicolith ....................................................................................................... 105 Calcified Lymph Nodes ........................................................................................................ 105 Splenic Artery Calcifications ............................................................................................. 105 Calcification of the Abdominal Aorta and of the Common Iliac Artery ......... 105 Monkeburgs Medial Sclerosis .......................................................................................... 105 Aneurysms ................................................................................................................................. 105 Ruptured Thoracic Aortic Aneurysms .......................................................................... 105 Calcific Foci in the Liver and Spleen .............................................................................. 106 Dermoid Cysts in Ovary (Teratoma) ............................................................................. 106 Uterine Fibroid ........................................................................................................................ 106 Adrenal Calcifications .......................................................................................................... 106 Pancreatic Calcification ...................................................................................................... 106 Porcelain Gallbladder/Cystic Calcification ................................................................ 106 Urinary Calculi ........................................................................................................................ 106 Calcifications in the Kidney ............................................................................................... 107 Nephrocalcinosis .................................................................................................................... 107 Nephrolithiasis ........................................................................................................................ 107 Bladder Stones ........................................................................................................................ 107 Prostate Calcifications ......................................................................................................... 108 Vas Deferens Calcification ................................................................................................. 108 Renal Cystic Calcification ................................................................................................... 108 Hydatid Cysts ........................................................................................................................... 108 Splenic Cysts ............................................................................................................................. 108 Solid Mass Calcifications .................................................................................................... 108 Mesenteric Lymph Nodes ................................................................................................... 108

RADIOLOGY REVIEW

9 Conditions for an AP lower C-Spine x-ray: include C3-T1 Magnification: If the structure is further from the film, the structures will be more magnified. If the structure is closer to the film, the structure will be less magnified. Pillar Hyperplasia (C/Spine): It is normal to have pillars that are thicker anteriorly than posteriorly. This contributes to the cervical lordosis. Some people have variation that that the posterior aspect of the articular pillars are thicker, creating a decreased cervical lordosis, however this is still NORMAL. In the picture, you can see that a pillars are thicker anteriorly than posteriorly. In b, the pillars are thicker posteriorly than anteriorly. This is called Pillar Hyperplasia. This is a normal variant. Canadian C-Spine Rules These are the rules to follow, when deciding whether to x-ray a patient with a cervical complaint. Does the patient have any of the following high risk factors? If you answer yes to any of these question, take radiographs. Age >65 Significant mechanism of injury (fall >1 m; axial load to head diving; high speed MVA; bicycle collision) Paresthesias in extremities

Dermoid Cysts/Teratoma .................................................................................................. 108 Uterine Fibroid/Leiomyoma ............................................................................................ 108 Condiut Wall Calcifications .............................................................................................. 109 Splenic Artery Calcification .............................................................................................. 109 Vas Deferens ............................................................................................................................ 109 Fallopian Tubes ...................................................................................................................... 109 Diverticular Densities .......................................................................................................... 109 Calcification of Abdominal Tumors ............................................................................... 109 Differential Diagnoses Lists for Abdomen ................................................................. 109

NORMAL RADIOGRAPHICAL APPEARANCES & THE BASICS

Intro to Cervical Spine & Some Basics
Complete upper cervical radiographic exam includes: APOM, AP lower cervical, and Lateral C-Spine. Oblique Views in C-Spine (these should not be routine). RAO (Right anterior oblique): right shoulder against bucky, marker is posterior to the spine on the film. RPO (Right anterior oblique): right shoulder against bucky, marker is anterior to the spine on the film. LAO (Left anterior oblique): left shoulder against bucky, marker is posterior to the spine on the film. LPO (Left posterior oblique): left shoulder against bucky, marker is anterior to the spine on the film. ASS & POO: Anterior oblique Same Side IVFs. Posterior Oblique Opposite side IVFs.

Does the patient have have any low risk factors allowing safe ROM assessment? If you answer no to any of these questions, have the patient imaged. If you answer yes to any of the below questions, can the patient rotate his/her neck 45 to the right and left? If they are unable to, the patient needs imaging. If the patient does have this ROM, no imaging is required. Normal cognition, no neurologic symptoms Simple rear end MVA Sitting position in waiting room Ambulatory at any time Delayed onset of neck pain Absence of mid-line C-spine tenderness

Introduction to Thoracic Spine

Complete thoracic radiographic exam includes: AP (end plates appear clear and crisp because of diverging rays) and the lateral thoracic spine view.

Search Pattern (ABCS): A (Air), B (Bone), C (Cartilage), S (Soft tissues).

 Thoraco-Lumbar Spot View: Is indicated if you accidentally cut off a region, if the patient has pain in a specific place, or if you require a tight view of a specific area. Lateral Thoracic View: On the lateral thoracic view, you will see hemi diaphragms. The crisper/cleaner hemidiaphragm is the diaphragm closer to the film, and the cross the spine at T12. Soft tissues of the arm normally block C7-T1. T7 Landmark: inferior angle of the scapula. Normal shape of the vertebral bodies in the thoracic spine: square. o There may be normal wedging near the lower thoracic spine.

10 Normal lateral bending/scoliosis in the thoracic spine: 10* of bending away from the heart (because of the location of the heart). Paraspinal soft tissue stripe: is on either side of the vertebrae. Swelling indicates: Trauma, Infection, Tumor. Upper vs Lower T-Spine Densities: The lower thoracic spine can be easily over penetrated, so use a screen in the upper T-Spine to compensate for the differences. Thoracic vertebrae morphologic characteristics = the vertebral height of the thoracic vertebral bodies is about 2-3 mm less anteriorly than posteriorly, which partially contributes to the thoracic kyphosis. Normal wedging of the lower thoracic vertebral bodies is common, especially in males. There is a wedging ratio is 0.8 in males and 0.87 in females at T8 to T12, and this is considered normal.

Swimmers View: Indications: To see the C7-T1 junction which can be obscured by the scapula, soft tissues and bones of the arm.

Introduction to Lumbar Spine

Normal Views: PA (use gonadal shields to protect reproductive organs) AP Lateral Obliques

Patient Positioning in thoracic spine views: Collimate to include T1-T12, TVPs and rib heads Have pt inspire to lower diaphragm.

How to evaluate radiographic quality: All appropriate segments should be included. Is there collimation? Is the radiograph over/under penetrated? Patient positioned correctly? Is there a marker? Is there a patient name on the film? Was there appropriate shielding (gonadal shield, half apron, full apron)

Lumbar Obliques allow you to see 3 things: the pars interarticularis, the posterior elements, and the facet joints. Both sides (RAO/RPO, LAO/LPO) are taken. ASS & POO rule does not apply. AP angled lumbosacral spot view (Hibbs View, tilt-up view) is indicated with sacroiliac joint pain, lumbosacral pain, and when there is bowel gas obscuring the L5-S1 region on the AP/PA lumbar view with evidence of abnormality in the area. Allows you to see L5, the upper sacrum and the sacroiliac joints. The AP Sacrum View shows the median crest of the sacrum (which is basically just fused spinous processes), the intermediate crest (which is made up of fused facets), and sacral foramina (which are the IVFs), the lateral crest (which is the fused TVPs) and the sacral hiatus (S4-S5). Number of lumbar segments Typically 5 But can have 4 or 6 and still be normal

How to measure thoracic kyphosis: Use the lateral thoracic view. Draw a line through and parallel to the superior endplate of T1. Draw a ling through and parallel to the inferior endplate of T12. Drop perpendicular lines to these two lines, and measure the resultant angle between these two lines.

Magenblasse: air in the fundus of the stomach. SPs in the Thoracic Spine: Should point inferiorly, over top of the vertebral body of the inferior vertebra.

Pars Interarticularis Found in the lumbar and thoracic spine.

RADIOLOGY REVIEW
In the cervical spine, there are articular pillars. Diverging Rays Usually the L3 endplates are seen clearly because the diverging rays go straight through the IVD. Normal view: AP Pelvis, AP Hip, and bilateral frog view of the hip (if pathology, no lateral) Intramembranous ossification: bones formed in fibrous membrane. Endochondral ossification: ossification proceeds around a cartilage template. This can include tubular bones, vertebrae and the skull. Used to lengthen bones after birth to skeletal maturity. Parts of bones = the physis is the growth plate, the diaphysis is the long shaft of the bone, the metaphysis is the widened part of the bone between the end of a long bone (the epiphysis) and the diaphysis. An apophysis is a place where the tendons attach to the periosteum of the bone. ZOPC stands for zone of provisional calcification, and is the junction of the physis and metaphysis, the region of calcification of the physis. When looking at PA Pelvis views and the SI joints, note that the MEDIAL line is the POSTERIOR SI joint. Muscle Attachments: Iliac crest = abdominal muscles. ASIS = Sartorius AIIS = rectus femoris Greater trochanter = gluteal muscles Symphysis pubis = adductor group Lesser trochanter = iliopsoas Ischial tuberosity = hamstrings

11

Things you may see in the lumbar view: Psoas shadow. The psoas muscle is a muscle deep in the abdomen against the spine. It is a powerful hip flexor that attaches to the femur. Bowel gas (Pringle calls this a Poopoma for fun)

PA View: Should see the Sacroiliac joint and the all the end plates clearly. AP View: Only the endplates hit by the central ray are seen clearly. You will see the sacroiliac joint duplicated. The anterior part of the joint is more lateral and the posterior part of the sacroiliac joint is more medial, making it look like two joints! Note: the superior 1/3 of the sacroiliac joint is fibrous, and the inferior 2/3 is synovial. This is important when determining what conditions can affect the sacroiliac joint. When should we be concerned about bowel gas? If the patient has back pain, or pain upon palpation in the region, or if the patient has a history of cancer. Intervertebral discs in the lumbar spine: the biggest IVD (intervertebral disc) is the L4-5 disc. The L5-S1 disc is normally wedged, and is the smallest. In the thoracic spine, the discs should NOT be wedged. How can you tell if the patient was positioned correctly of if the patient was rotated on the radiograph? Compare the spinous processes to the pubic symphysis. They should be in line with each other. The air shadow of the gluteal clefts should line up straight with the pubic symphysis. The pedicles should be straight. Sometimes the spinous processes will vary in direction

Introduction to the Knee

There are four normal views in a limited series of the knee: AP Tunnel Lateral Tangential (Sunrise)

Hadleys S-Curve: inferior aspect of the TVP, superior aspect of the facet, and superior aspect of the TVP.

Introduction to Pelvis
Indications for taking this view include: trauma to the pelvis, trauma, and pathology.

 You should be able to identify the following structures: femoral shaft, adductor tubercle, lateral epicondyle, medial epicondyle, popliteal groove, intercondylar notch, tibial tuberosity, intercondylar eminences, medial tibial condyle (plateau), lateral tibial condyle (plateau), styloid process of the fibula, neck of fibula, tibial shaft, fibular shaft and the patella. The infra and suprapatellar fat pads sit in front of the knee and will appear as lucencies, and indicate trauma. They show that the soft tissues have been distended and the fat pads have been pushed out. Use the Tangential/Sunrise Patellar View to assess the patello-femoral joint. It is common to see dislocations of the patella towards the lateral aspect. In the pediatric knee, you should be able to see growth plates, and with kids you ALWAYS want to take a bilateral view!! Ottawa Knee Rules Do a knee x-ray series if the patient present with any one of the following findings: Age >55. Tenderness of the patella (and only the patella). Tenderness of the fibular head on palpation. Inability to flex the knee 90. Inability to bear-weight on the affected limb immediately and in the emergency department (4 steps, unable to transfer weight twice on each leg).

12 Medial oblique Lateral

Please be able to locate these structures: tibia, medial malleolus and lateral malleolus, plafond of the tibia, tibiofibular joint, sinus tarsi, anterior tubercle of the calcaneus, posterior tubercle of the calcaneus, sustentaculum tali, metatarsals, phalanges, sesamoids, fibula, ankle mortise, the head, neck and body of the talus, the calcaneus, the navicular bone, cuboid bone, subtalar joint, the three cuneiforms and the tarsometatarsal joints. The sustentaculum tali is seen on the lateral view. It is a horizontal eminence of the upper and forepart of the medial surface of the calcaneus. The plantar calcaneo- navicular ligament, tibiocalcaneal ligament and medial talocalcaneal ligaments attach to the sustentaculum tali. The tibial plafond is a joint surface of the distal tibia at the ankle. This term is radiology- specific. The Navicular articulates with the 1 -3 cuneiforms which lead to the metatarsals. The th th cuboid articulates directly with the 4 and 5 metatarsals. The ankle mortise is the actual ankle joint, made up of the tibia and fibula articulation. The fibular notch is an indentation in the tibia where the fibula articulates. When looking at the lateral foot radiograph, always remember that if you see the lateral part of the foot more clearly, this is the medial oblique view!! If you see the medial part of the foot more clearly then it is the DP view!!!! Indications for MRI of the knee: Meniscal degeneration and tears Anterior Cruciate Ligament disruption Posterior cruciate ligament disruption Collateral ligaments injury Chondromalacia Patellae Extensor mechanism abnormalities (patellar tendonitis, patella alta and baja, patella bursae. Ganglion cyst, meniscal cyst, synovial cyst. Fractures/bone bruise
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Exclusion criteria includes: Age <18 YOA. Isolated superficial skin injuries Injuries >7 days old Recent inuries being re-evaluated Patient with an altered lecel of consciousness Paraplegia Multiple injuries

Introduction to the Ankle & Foot

There are three views in a limited series of the ankle: AP Lateral Medial Oblique

Normal views in a limited series of the foot: DP (dorsoplantar)

Advantages of MRI of the Knee: non-invasive, comprehensive, very accurate. C-Sign: This is also known as the Anteater Sign, which suggests talocalcaneal coalition. You will see continuous trabeculae through the areas of fusion.

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Ottawa Ankle Rules X-rays of the ankle are required when there is bony pain in the malleolar/midfoot region associated with any one of the following: Tenderness along the distal 6 cm of the posterior tibia or tip of the medial malleolus. Tenderness along the distal 6 cm of the posterior fibula, or tip of the lateral malleolus. Tenderness at the base of the fifth metatarsal. Tenderness at the navicular bone. Inability to bear weight immediately and in the emergency room for four steps.

13 The acromiohumeral space (7-11 mm) is the space where the supraspinatus runs through. If you see calcification in this space, this indicates calcific tendonitis from rotator cuff injuries. Also, if you see this joint space severely decreased with the humeral head migrating superiorly, this usually indicates a rotator cuff (supraspinatus) tear resulting in the deltoid muscle taking over and pulling the humeral head superiorly towards the acromion. In the coracoclavicular space (11-13 mm), an increase in this space can be seen in AC joint injuries where the clavicle will elevate because the holding element within the joint has been disrupted. In the internal rotation view, you will see that the greater and lesser tuberosities are rotated, and your x-ray beams are shooting right through the greater and lesser tuberosities. You will see the greater tuberosity that appears lucent, and the lesser tuberosity that now sits on the medial aspect of the humerus. You might say that the humeral head looks like a scoop of ice cream sitting on a cone (the humerus). If you think of it this way, the greater and lesser tuberosities form the outer borders of the ice cream scoop, and the cone is the humerus. You may see the greater tuberosity end on in the internal rotation view which will make it look like a cystic lesion do NOT hallucinate the normal appearance of the greater tuberosity seen end-on into a tumor or a cyst!! This is normal because there is less trabeculation in the greater tuberosity region. In the baby arm view, the greater and lesser tuberosities are sharply marginated and almost overlapping each other. The AC joint may appear dark on some films. You may see another pseudocystic tumor from the greater tuberosity. Remember, if it is well demarcated, and has continuous margins it is likely benign or normal, in this case, its normal! An os ascromiale is an extra little boney ossicle, which is completely normal. It is a supernumery (extra bone) or secondary ossification center that did not fully fuse. This is normal if the person is not skeletally mature, so you must remember to look at the age of your patient. In an adult, it should be well corticated to be benign. Os acromiales will not cause pain, and it is not floating around like you might think, there is cartilage around it holding it in place. There are additional views of the shoulder that can be taken: the axillary view of the shoulder, the Y view of the scapula, and uni/bilateral clavicle views. The axillary view of the shoulder is taken with the patients arm abducted, and the x-ray beam shot through the axiilla up towards the cassette. The AC joint and clavicle are

Exclusion criteria include: <18 YOA. Pregnant women. Patient with diminished ability to follow the test (i.e. head injury or intoxication).

Introduction to the Shoulder

There are three normal views in the shoulder series: AP internal rotation, AP external rotation and baby arm view. Remember, that you always want views at 90 to each other. We use the internal and external rotation because you want perpendicular views. In these three views of the shoulder we reviewed the following structures: coracoid process (inferior to the clavicle laterally), acromion process, clavicle, glenoid fossa, spine of the scapula, posterior ribs and anterior ribs (the posterior ribs angle down and the anterior ribs wrap around and will appear larger than the posterior ribs due to angulation), lung apex and lung fields, pectoralis groove, coronoid tubercle, acromioclavicular joint, head of the humerus, glenohumeral articularion, greater tuberosity (more lateral than the lesser), lesser tuberosity (more medial than the greater), intertubercular (bicipital) groove (houses the biceps tendon), anatomical neck of the humerus (the region right adjacent to the humeral head, is obliquely oriented) and surgical neck of the humerus (is just distal to the anatomical neck, and is the most common place where fractures occur due to instability of this area, and it is also the part of the humerus surgeons will fracture if they need to, this is the part of the humerus where the shaft begins and the metaphysis narrows into the diaphysis), shaft of the humerus, physis scar, and the superior angle, vertebral border, axillary border and inferior angle of the scapula. If you dont recall these, go to pages 136, 139 and 141 of Yochum and Rowe and refamiliarize yourself with these structures.

 anterior (at the top of the x-ray), while the bottom is considered posterior. You will be able to see dislocations with this view. Most commonly the humerus is dislocated anteriorly, only sometimes posteriorly (which are difficult to view on the AP). Also look for subtle fractures on this view. The Y view of the scapula is used for traumatic fractures and dislocations as well, looking down the body of the scapula through the shoulder. The Y is formed by the body of the scapula, coracoid process and spine of the scapula with the acromion. The center of the Y is where the glenoid will be (which houses the humeral head). If the humeral head is not centered in the glenoid, suspect a disocation or subluxation of the glenohumeral joint. This view shows you a true lateral view. If the patient were having clavicle pain, you would use the uni or bilateral clavicle view. With this view you can see the space between the coracoid and the inferior-most part of the clavicle, however this space will seem narrow in this view because of tube angulation. Evaluate all joint margins, spaces, and note any lysis/destruction of the distal clavicle with increased joint space! Well talk about what this means later, you will have to wait in anticipation until we get there! But to make you sound smart this is called acro-osteolysis of the clavicle (or osteolysis of the distal clavicle, acro = the distal end).

14 assess the surrounding structures and soft tissues! You don not want to confuse this with AVN (avascular necrosis = death of bone from lack of blood supply) or trauma.

Introduction to the Wrist

There are four views in a minimal diagnostic series of the wrist: the PA, medial oblique, lateral and PA with ulnar deviation for all trauma patients. The PA with ulnar deviation view allows for better visualization in and around the scaphoid. We looked at the following structures in these views: the scaphoid, lunate, triquetrum, pisiform, trapezium, trapezoid, capitate, hamate and hook of the hamate, radial styloid, radioulnar joint, radiocarpal joint, carpal arches, pronator quadratus fat plane, ulnar styloid, metacarpals, intercarpal joints, carpometacarpal joints, phalanges, and the navicular fat stripe. There is an acronym to remember the carpal joints: Some Lovers Try Positions (all in the proximal row) That They Cannot Handle (distal row). The proximal row carpals (from medial to lateral) are: scaphoid, lunate, triquetrum and pisiform, and the carpals in the distal row (from lateral to medial) are: hamate, capitate, trapezoid, and trapezium (UM = THUMB). The scaphoid is the bone that looks like snoopy, or a duck that sits and overlaps the lunate. The capitate sits above the scaphoid, and the triquetrum sits above the head of the duck (scaphoid). Ulnar deviation is a common problem in those patients who slip and fall on an outstretched hand. Terry Thomas Sign is when there is a space between the scaphoid and lunate. DISI (Dorsal intercalated segment instability: when the lunate is dorsally tilted, and the scapholunate angle (30-60) increases. VISI (Ventral intercalated segment instability): occurs when the lunate is tilted in the volar direction, decreasing the scapholunate angle (30-60). The order of appearance of the carpal bones: Progresses in a circle: Capitate Hamate Triquetrum Lunate Scaphoid Trapezium Trapezoid Pisiform

Introduction to the Elbow

There are four normal views of the elbow in a limited series: the AP view, medial oblique, lateral and tangential (Jones) view. We looked at some structures on the humerus that you should know for this view: trochlea, capitellum, lateral epicondyle, medial epicondyle, olecranon fossa, coronoid fossa, shaft, and the supracondyar ridge. On the ulna we looked at the coronoid process, olecranon process, and trochlear notch. On the radius we was the radial head and neck, tuberosity, the articular surface head and the shaft. You must know the order of appearance of the secondary ossification centers of the elbow. The mnemonic is CRITOL(E). C = Capitellum (first to appear, long before the others, usually within the first 6 months) R = Radial head I = Internal/medial epicondyle T = Trochlea O = Olecranon process L (E) = Lateral/external epicondyle

You can have multiple centers of ossification, which can look jagged or irregular. Look at the opposite side to compare because a lot of these asymmetries can be bilateral. Also

RADIOLOGY REVIEW
Ulnar Negative Variance: when the length of the ulna relative to the length of the radius is different. The ulna is unusually short in this case and the triangular fibrocartilage (TFCC) is thicker. There may be an increased risk of AVN at the lunate/Keinbocks Disease (but this is controversial) and impingement syndrome. Ulnar Positive Variance: when the length of the ulna is longer relative to the radius, and is associated with tears of the TFCC (triangular fibrocartilage) and ulnar impaction syndrome. This can cause more wear and tear in this area degeneration. Os Styloideum: an accessory ossicle present at the base of the 2 metacarpal and 3 th metacarpal (sometimes), in 1-3% of patients. This was formerly believed to be a 9 nd carpal bone. An os styloideum likely comes from the non-union of the developing 2 metacarpal styloid process. Patients will present with a carpal boss (painful lump over dorsum of wrist). Carpe Bossu Disease/Syndrome is characterized by insidious onset of pain at nd rd the base of the 2 and 3 metacarpals, which is exacerbated by movement. There may or may not be associated with premature osteoarthritis in the region of the os styloideum. Carpe Bossu Disease is found in 33% of patients with a carpal boss.
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15 fuse together by the age of 3 in the cervical spine to complete fusion by age of 6 in the lumbar spine. There are secondary ossification centers that will fuse by age 20-25. They include the ring apophysis (epiphysis) that appear by age 9 in the upper and lower end plates. There are centers for the TVPs and SPs that appear around puberty. The lumbar vertebrae have centers for the mammilary processes. Skeletal maturity charts can be used to help compare chronological age with skeletal maturity. There are 7 secondary ossification centers on each vertebra. There is one on each TVP (2), one on each inferior articular facet/process (2 superiorly and 2 inferiorly), and one on the spinous process (1). There are two types of ossification: intramembranous and endochondral ossification. Intramembranous ossification is when bones form in a fibrous membrane. Endochondral ossification is when there is a cartilage template that precedes ossification, and is used to lengthen long bones after birth to skeletal maturity. Endochondral ossification occurs in tubular bones, vertebra, and the skull (among others).

Indications to X-Ray Kids for back pain

Assess the patient with a thorough history and physical examination. There are 7 warning signs: 1. 2. 3. 4. 5. 6. 7. 8. Age <4 YOA Back pain causes functional disability. Duration of pain is > 4 weeks. Fever Postural shift of the trunk. Limited movement because of the pain. Neurological abnormalities. History of significant trauma with immediate onset of pain.

The Pediatric Spine

Characteristics: in the pediatric spine, there will be Hahns clefts (vascular notches), unfused neurocentral junction, an oval shaped vertebral body shape, and a lack of lumbar lordosis before the child is weight bearing (walking).

The Skull
Recently, CT and MRI have replaced radiographs of the skull. DCs shouldnt be x-raying the skull unless they do it regularly and know the anatomy well. The minimal diagnostic series include both right and left lateral views, the PA (Caldwell) eye and ear view, Townes View (Occiput, foramen magnum, dorsum sellae and petrous ridges), the Skull Base View (submentovertex or erticosubmental, to see the base of the skull, foramina, petrous ridges, sphenoid sinus, atlas and dens, and Waters View allows us to see the paranasal sinuses.

How to position kids for x-rays: you can use restrains, or use the parents to help hold the child down, or in extreme cases, sedation can be used (for MRI or CT). Do NOT hold the child yourself, or have one of your staff hold the patient. Always get a family member to hold the child down if necessary. How do vertebrae develop? In the lumbar spine, there are 3 primary ossification centers, one in the vertebral body (centrum), one for each side of the neural arch (two). th These usually appear by the 8 fetal week. The neural arch fuses by the end of the first year of life, starting in the lumbar spine. The neural arch and the vertebral body will

ROENTGENOMETRICS
Defn: Measurements on the radiograph via lines and marks on the radiographs. Include 2 mm of error in either direction (positive & negative).

Cervical Spine Roentgenometrics

ADI (Atlanto-Dental Interspace) is the space between posterior portion of anterior tubercle of C1/Atlas, and the anterior part of the odontoid process. It should be 1-3 in

 adults, and can be 1-5 in kids. This distance should not change with movement. The ADI can increase with age (from degeneration of the atlantodental joint), trauma (rupture of the transverse ligament), Downs Syndrome (the transverse ligament can be lax), and Inflammatory Arthropathies (Rheumatoid Arthritis, Psoriatic Arthritis, Reiters Syndrome, and Akylosing Spondylitis). Cervical Lordosis: Draw a line along the C1 plane, and another along the inferior end plate of C7, Draw a line perpendicular to each of these lines, and measure the resulting angle. The normal cervical lordosis is 35-45*. In the absence of trauma, there is no evidence that a decreased lordosis has any clinical significance. Cervical Stress Lines: A line is drawn from the back of C2 and the back of C7. At the point of their intersection is the focus of the stress. This is of unknown significance. Chamberlains Line: is a line drawn from the posterior hard palate to the posterior lip of the foramen magnum. If the dens is >3mm above the line this indicates basilar invagination. Eisensteins Measurement: is the saggital diameter of the spinal canal, the space between the spinolaminar line and the posterior part of the vertebral body and is used to detect cervical spinal stenosis. If the measurement is <15 mm, this suggests stenosis may be present. If the measurement is <12 mm, then this indicates definitively that stenosis is present. Georges Line: runs along the posterior margins of the vertebral bodies. This line should be smooth and unbroken. It should line up at every level and the vertebra should stack up nicely on top of each other. McGregors Line: is a line drawn from the upper surface of the posterior end of the hard palate to the most caudal point of the occipital curve of the skull (the most inferior part of the occiput). The dip of the dens should not project above this line more than 8 mm in males and 10 mm in females. If the dens projects more than 8 mm (males) or 10 mm (females), this indicates basilar impression.

16 Retropharyngeal interspace: is the space between the pharynx (from C2-C5) or the trachea (from C6 to lower) and the anterior border of the vertebral bodies in the lateral lower cervical view. From C2-C5 (behind the pharynx) the maximum distance should be 7 mm. From C6 and lower (behind the trachea) the maximum distance should be 20-22 mm. If the retropharyngeal interspace is larger than these measurements, this can indicate TIT (Trauma, Infection or Tumor). Retrotracheal interspace (at C7) = the upper limit is 7 mm. Spinolaminar line: runs along the border between the lamina and the spinous processes. This line should be smooth and unbroken. There is one exception: at C2 the spinolaminar line may be 2-3 mm posterior from C1 because C2 has a very long spinous process. In this case, check the alignment of C1 with C3. Steeles Rules of Thirds: 1/3 of the space within the atlas is for the dens, 1/3 is for the spinal cord and brain stem, and 1/3 of the space is free space. Stable vs unstable radiographic criteria on the lateral cervical spine = 3.5 mm horizontal translation on the lateral cervical spine. 11 degrees or more of angular deformity between two adjacent vertebral segments.

Thoracic Spine Roentgenometrics

Thoracic Kyphosis: Is measured by drawing a line along the T1 superior end plate and another along the superior endplate of T12, and then drawing lines perpendicular to each of these lines. Determine the angle between these two lines. Normally, the thoracic kyphosis should be 20-40. Georges Line: is used to see if the vertebrae are stacked properly in the thoracic spine. Similar to Georges line in the cervical spine.

Lumbar Spine Roentgenometrics

Interpedicular Distance: is the minimum distance between the pedicles on the AP/PA view. As you look inferiorly along the spine, this distance should increase (except in Achondroplasia Dwarfs). At L1, the distance can be 21 mm (min) to 29 mm (max). At L5, the min distance is 23 mm to a max of 36 mm. Lumbar Gravity Line: is determined by drawing a vertical line from the L3 body center and vertically down. The line should pass through the anterior 1/3 of the sacral base. Lumbar lordosis: is determined in the same was you would measure the thoracic kyphosis or cervical lordosis. The normal angle is 50-60.

RADIOLOGY REVIEW
Lumbar Stability: if there is >3.5 saggital excursion from full flexion to full extension then this indicates instability. >11 in lumbar angular motion indicates instability. 75% of saggital body diameter movement using Henderson and Dorman templating method. Lumbosacral Disc Angle: is the angle between L5 and S1, and normally should be 10-15. The disc angles decrease as you move cephalad. Presacral Space: is the prerectal space (retrorectal space) = maximum 2 cm Sacral Base Angle/Fergusons Angle/Lumbosacral angle: is the angle of the sacrum to horizontal. It should be 26-57.

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Shoulder Roentgenometrics
Glenohumeral joint space: 4-5 mm. Acromioclavicular joint space: 2-4 (5) mm. Acromiohumeral joint space: 7-11 mm. This joint space should be measured on the external rotation view. The supraspinatus runs through this space. Calcific tendonitis can be an indirect indicator of a rotator cuff injury, causing the deltoid to migrate superiorly, decreasing this space. So if you see the AH joint space decreased, think RC injury/tear! If you see this space increased, this is likely due to excessive inflammation. Coracoclavicular joint space: 11-13 mm. This space can increase if there is any sort of injury to the AC joint, causing the clavicle to elevate. Remember that the acromiohumeral and the coracoclavicular joint spaces are known as potential spaces, and the acromioclavicular joint is a synovial joint.

Foot Roentgenometrics
Boehlers Angle = if the angle is less than 28, a sign of calcaneal compression fracture.

Sacral Spine Roentgenometrics

Presacral/retrorectal space: is the space behind the rectum and in front of the sacrum. It should be no larger than 2 cm.

Elbow Roentgenometrics
Anterior humeral line: a line drawn along the anterior aspect of the distal humeral shaft in the lateral elbow view. This line should go through the middle third of the capitellum. This line is most commonly used when assessing for fractures. Radiocapitellar line: this line is drawn along the central axis of the radius and should pass through the centre of the capitellum. This line is typically used when assessing for dislocations.

Pelvic Roentgenometrics
Kohlers Tear Drop Distance: is the distance from the lateral margin of the pelvic teardrop to the medial part of the femoral head on AP pelvic x-rays. It should be no larger than 11 mm, and if it is, this is termed Waldenstroms Sign. The maximum difference between right and left is 2 mm. Shentons Line: is the curve along the upper margin of the obturator foramen that continues inferolaterally below the margin of the femoral neck in the medial aspect of the femoral shaft (on the AP pelvic view). This line should be smooth and unbroken. Symphysis Pubis Width: is the distance between the right and left medial ends of the pubis bone. It should be 6-7 mm in adults, and if its wider, this indicates diastasis of the pubis symphysis. Iliopubic lines = the anterior column of the pelvis. Ilioischial lines = show the posterior column of the pelvis. Anterior and posterior acetabular rims = the anterior rim is more medial and the posterior rim is lateral. Teardrop distance = summation of shadows of the medial acetabular wall.

Wrist Roentgenometrics
Scapholunate angle: a line through the long axis of the lunate and the long axis of the scaphoid. Normally should measure 30-60. Anything above or below this angle suggests a dislocation.

Pediatric Pelvis Roentgenometrics

Ischiopubis synchondrosis: is the cartilaginous joint in a child between the ischium and the pubis. It should fuse between 4-8 YOA. Rissers Sign: Is a sign that uses the iliac crest epiphysis, and is a grading system used as an indicator of skeletal maturity and is especially important and helpful for scoliosis patients. It first appears laterally near the ASIS and moves posterlaterally toward the PSIS. It appears at 14 YOA in girls and 16 YOA in boys. It should completely fuse and be fully formed in 3-4 years after its initial presentation. It takes 1 year to cap, and 2-3 years to completely fuse after that. Grade 1: 25% fused (ossified)

 Grade 2: 50% fused Grade 3: 75% fused Grade 4: nearly 100% fused Grade 5: 100% fused *Zylich from peds class: Grade 1: 25% ossified Grade 2: 50% ossified Grade 3: 75% ossified Grade 4: 100% ossified Grade 5: Fusion

Triradiate cartilage: is where the ischium, ilium and the pubis join in the hip joint socket. The three bones form a Y shape and fused by 13-15 YOA (puberty).

IMAGING MODALITIES
Bone Scans (Scintography)
Uses an IV to inject Technetium-99 (a radioactive nuclide emitting gamma ray), which will concentrate with increased blood flow/osteoblastic activity. Bone scans are sensitive, but not specific. Conditions which may produce a hot bone scan include fracture, most malignancies, some benign tumors, infection, arthropathies, AVN, and Pagets Disease.

18 indicated with trauma, osseous spinal stenosis, lumbar disc herniations (almost as good as MRI for herniations) and patients with implantations who cannot have an MRI. Hounsfield units are used. There two windows used for CT: a bone or a soft tissue window. The window level is the intensity that represents the center of the window width (WW). WL (window level) is selected to focus on a specific tissue type to enhance the image accordingly. Soft tissue windows have window levels of 0-200, and bone windows have window level (WL) of 250-500. The window width (WW) is the number of shades of grey included on the window. In the soft tissue window, the WW is 200-600. In bone windows, the WW is 1000-2000. When taking images of the lumbar spine, you must see L3-S1 (max). There should be contiguous slices, and the radiation does is approximately equal to doing a 5 view lumbar spine series, depending on the slice thickness. Images are all in the axial plane. When viewing CT images, they are viewed as though the doctor is standing at the patients feet with the patient is lying supine. Divide the spine into 2 areas: the level of the IVF and the level of the pedicle. The level of the IVF includes the disc, vertebral body, facets and ligamentum flavum. The level of the pedicle includes the pars interarticularis and transverse processes. We looked at notochordal remnants on CT (Cupids Bow), Schmorls Nodes, and Achondroplasia (the canal dimensions at L5 can be decreased by 50%). CT is great for looing at bony structures and conditions including osseous stenosis, degeneration (i.e. GREAT for degeneration of facets), and fractures. Because CT uses ionizing radiation (like x-ray), cortical bone will always be WHITE. In the bone window, you will see bony detail, and you should be able to differentiate between medullary and cortical areas. Soft tissues will not be visualized well. In the soft tissue window, you will be able to see the soft tissues better, and the bone will be chalky-white. You will not be able to differentiate between medullary and cortical bone.

DEXA (Dual Energy X-ray Absorptiometry)

Used to determine bone density, and is great for patient with OP. This is the gold standard for assessing bone density. This is good because there is a low radiation dose. Imaging is not diagnostic, you must look at the T-scores and Z-scores. The T-score compares your patient to a healthy cohort (Terrific Group), for example this score compares your patient to a healthy cohort. If the t score is > -1, this indicates normal bone density. If the T score is between -2.5 and -1 this indicates osteopenia (Op), if the scores is less than -2.5 this indicates osteoporosis (OP) and if the score is -2.5 or below with the presence of a fracture this indicates severe osteoporosis. The Z-score compares your patient to a bunch of other patients in the same cohort (The Zame Group.), for example, if you had a 25 YO patient, the z-scores compares your patient to a group of 25 year olds. If the z-score is higher than -1, then the patients bone mass is within or above the normal range for the patients age. If the z-score is between -1 and -2.5, the bone mass is lower than the average for the patients age, and if the z-scores is less than 2.5, then the patients bone mass is much lower than the average for the patients age.

MRI
Stands for magnetic resonance imaging. MRI uses a magnet, hydrogen protons, external radiofrequency and sequence selection. It does not use ionizing radiation, and images can be taken in any plane. MRI can take images of larger sections of the body and there are no dangerous contrasts used. However, MRI has many high false positive rates and is more expensive. In patients with MRI imaging, there were nearly identical outcomes for primary care patients with LBP. There are two pulse sequences, T1 and T2. T1 is the fat image, and lots of white is seen. It is good for seeing anatomy and can be enhancable with gadolinium. Two is the water image (H20), you will see structures with high water content (structures with high water contact have high signal intensity), fat is suppressed on T2 images. Contraindications for MRI include: cardiac pacemakers, dorsal column stimulators, prosthetic heart valves, intra-cranial vascular clips, those dependent on other mechanical electrical or magnetic apparatus, metallic intra-ocular foreign bodies, vascular clips anywhere less than 2 weeks after insertion unless they are MRI compatible (these are all mainly due to the magnetic usage of MRI). Possible contraindications include: unstable/monitored patients possibly needing resuscitation,

CT (Computed Tomography)
CT Is fast, has detailed bony anatomy and is ideal for surgical planning. However it uses ionizing radiation, and is not good at assessing soft tissue and contrast is needed. CT is

RADIOLOGY REVIEW
patients with artificial eyes, if the patient is too large or heavy, if the patient is in severe pain and may move around, if the patient is claustrophobic, pregnant women, local heat (around metallic implants, but this has not been shown to be harmful), and possibly tattoos or permanent eyeliner. Indications for spinal MRI include: lumbosacral radiculopathy, spinal cord abscess, spinal infection, spinal stenosis, nontraumatic vascular injuries of the spine, tumors, myelopathy , multiple sclerosis and cauda equina. MRI allows you to see ST changes, effusions, and neurological changes in the cord and brain very well. When looking at an MRI, cortical bone will be BLACK. In the T1 images, fat will be white (so look at the subcutaneous fat layer on the back), the spinal cord is dark, and bone will be bright/white (since its filled with fat). T2 images will show water as white. The spinal cord/thecal sac is white (because its filled with watery CSF. To help, use this little trick: T2 = H20.

19 (50% of cases), possible fusion or malformation of the spinous processes, and IVFs can be either smaller or larger. Clinical significance: Congenital blocks are rarely symptomatic. However, there will be no motion at the blocked segments. To compensate, there will be hypermobility above and below the block leading to premature degenerative disc disease (DDD)/degenerative joint disease (DJD). There may be associated organ anomalies. Management: Do not adjust bony fusions. The small IVFs are not significant in this case since the patient was born with the condition, the nerve root will not be compressed.

Acquired Block Vertebrae

When 2 vertebrae are joined together, similar to congenital block, however the vertebrae are joined due to pathological processes, not congenitally.

SKELETAL ANOMALIES
Dens Anomalies and Fractures
There are four different types of dens anomalies: agenesis (where the dens did not form), hypoplasia (the dens did not grow enough), os odontoidium (the dens is no longer attached to C2) and ossiculum terminali (where the tip of the dens is not formed). Agenesis and os odontoideum are not stable. There are three types of dens fractures

Klippel-Feil Syndrome
This is when there are multiple blocked vertebrae (>2) within the same region. Klippel- Feil Syndrome can occur in the cervical, thoracic or lumbar regions. Radiographic Findings: There is a triad of symptoms: 1. 2. 3. Short webbed neck Low posterior hair line. Reduced cervical ranges of motion

Congenital Block Vertebra

Fusion of 2 adjacent vertebrae (failure of segmentation) because of a lack of blood th supply during the 3d-8 week of fetal development. It is most common in the cervical spine. Common locations include C2-3, C5-6, T12-L1 and L4-5. Radiographic findings: Decreased AP diameter of the vertebral bodies (Wasp Waist Deformity), Remnant disc space/hypoplastic disc space, possible fusion of the facets

Clinical Significance: Decreased range of motion in the affected shoulder. There may be an associated torticollis, and facial asymmetry. Klippel-Feil is often associated with scoliosis, sprengles deformity, spine/rib anomalies, renal/GU, cardiac problems, and premature hearing loss. Management: Theres not much we can do for these patients other than refer out. The condition can be repaired surgically.

Omovertebral Bone

 This is a bone that runs from the C5-6 SP-Laminae, or the TVPs to the superior angle of the scapula. It is commonly associated with Sprengels Deformity cases. Radiographic Findings: Bony/cartilaginous/fibrous tissue running from the C5/6 SP/Lamina/TVP to the superior angle of the scapula

20 Management: Cannot adjust C0-C1.

Spina Bifida Occulta/Schisis Defect/Cleft Spinous

Is the non-fusion of the posterior arches at the posterior tubercle. More common in males, and at the L5/S1 level. Radiographic findings: Non-union of the posterior elements at a level. If at C1, possible stress hypertrophy of the anterior tubercle. Clinical significance: Possible spinal cord anomaly. Diagnosis cannot be made until age 12 because the normal spinolaminar ossification is not complete until then, and L5-S1 are the last spinal segments to do so.

Sprengels Deformity
This is a congenital elevation of the scapula. At the rd 3 fetal week of development, the scapula will fail to descent. Usually unilateral. Radiographic findings: the scapula is hypoplastic, shortened vertically, and broad. It may be rotated so the glenoid is rotated inferiorly. Clinical Significance: The deformity will not progress. Management: Conservative treatment (including physical therapy) will not improve the condition. Surgical intervention warranted for patients between the ages of 4 and 7.

No Name Anomaly
Concave facets with a notch on the medial portion of the lateral masses.

Calcification of the Stylo-Hyoid Ligament

When the stylo-hyoid ligament calcifies. Clinical significance: May be associated with Eagle Syndrome (difficulty swallowing). :

Posterior Ponticle/Pons Ponticus

Is a common condition, affecting 15% of the population. If the ossification or calcification of the oblique portion of the atlanto-occipital membrane that bridges the posterior lateral mass and posterior arch. Forms the peripheral border of the arcuate foramen with the vertebral artery and veins, first cervical nerve, and perivascular sympathetic nerves. Radiographic Findings: Partial/complete calcification/ossification of the atlanto-occipital membrane forming a partial/complete foramen at the ventral/superior aspect of the vertebral arch. Clinical Significance: Can be associated with migraine headaches without the aura. Management: Possible contraindication to manipulation.

Unfused Secondary Ossification Centers for Spinous Processes

Radiographic findings: Look for smooth cortical bone that lines up with the spinous processes.

Pedicle Agenesis
Sclerotic contralateral pedicle. (Diagnostic hallmark)

Facet Tropism
Asymmetry between the planes of the facets seen on AP/PA L-spine films. Most common at L5-S1. Clinical Significance: Assess the patients ability to rotate.

Butterfly Vertebrae
Failure of the ossification centers of the vertebra to unite. Most common at the thoracic spine and lumbar spine. Radiographic findings: a small increase in the interpedicular distance. Pedicles may appear enlarged. Adjacent endplates remodeled around the butterfly vertebra.

Paramastoid/Epitransverse Process
When the C1 TVP articulates with the skull, or forms a bony union. Radiographic findings: A bony projection from the jugular process of the occiput to the C1 TVP. Clinical Significance: Reduced ROM at the Occiput (C0)-C1 articulation.

RADIOLOGY REVIEW
Clinical significance: insignificant if it is an isolated anomaly. May see organ anomalies and spinal stenosis. This is a symmetrical anomaly, therefore there will be no resulting scoliosis.

21 Clinical Significance: Most patients never develop back pain. However, the patient may present with tight hamstrings, an achy lumbar spine when standing in one place or slow walking. There may be a palpable step defect and a hyperlordotic lumbar spine.

Scheuermanns Disease
Usually presents at ages 13-17, usually in males, and in the mid/lower thoracic spine. It is found in <5% of the population, and is familial. Radiographic findings: Irregular endplates and anterior wedging of at least 5 in at least 3 contiguous segments in the thoracic spine resulting in hyperkyphosis. Loss of disc height. Wide vertebral bodies. In children with Scheuermanns Disease, you will see associated pars defects. Clinical Significance: pain, fatigue, defective posture, or can be asymptomatic. Rigid hyperkyphosis in the thoracic spine. Hyperlordosis in the lumbar and cervical spines. Protuberant abdomen. Hypertonic hamstrings/iliopsoas, and pectoral muscles.

Hemivertebra (HV)
There are three types of hemivertebrae: Lateral HV (most common, occurs when the lateral ossification center fails to grow), Dorsal HV (rare, when the anterior portion of the vertebral body is absent), and Ventral HV (very rare, absent posterior part of the vertebral body). HV are most common in the thoracolumbar region. An Incarcerated HV is a hemivertebra that is fused to an adjacent segment. A non-incarcerated HV is when the disc space is interposed. Bizarre Differentiation of the Spine/Scrambled Spine is characterized by multiple HV and Block Vertebrae. Clinical Significance: This anomaly usually occurs in multiples, and there are often other bony and organ anomalies associated. If you have only one HV, then there will be a C- shaped scoliosis created as a result. If two hemivertebrae present, an S-shaped scoliosis will result.

Spondylolisthesis
Is the anterior displacement of a vertebral body in relation to the segment below. There are five types. Type 1 is Dysplastic (rare). Type 2 is Isthmic (pars defect). Type 3 is Degenerative (most common in females >50, at L4). Type 4 is Traumatic (also rare). Type 5 is pathological (rare, ex: cancer). Sponylolisthesis usually develops in childhood from repeated microtrauma. Displacement after 18 YOA is rare. Radiographic findings: When one vertebrae slips anterior in relation to the segment below. This can be graded into 4 grades using Meyerdings classification. Grade 1 represents a slippage of 25%. Grade 2 has 50% slippage. Grade III is a 75% slip. Grade IV is 100% slip. If the vertebra falls completely off the inferior vertebra, this is known as spondyloptosis. If the segment slips >25% (Grade I or higher), par defects are present whether they are seen on x-ray or not. If the spondylolisthesis is at L5, pars defects are usually present no matter what Grade the slippage is. May see bone growth on the sacral base with a L5-S1 spondylolisthesis, known as buttressing.

Hahns Clefts
Presence of vascular channels in the central portion of the vertebral bodies. Most common in the thoracic spine. Radiographic findings: lucencies (usually anteriorly) where vasculature enters into the vertebra.

Notochordal Remnants/Nuclear Impressions

Radiographic findings: a smooth and undulating curve involving almost the entire endplate, usually the inferior endplate but can involve the superior endplate. This is different from Schmorls nodes: Schmorls nodes are abrupt, and look like you poked your finger into the vertebral body. Notochordal remnants are smooth and curved impressions in the vertebral body.

22 Clinical Significance: If spatulated/fused TLSV, decreased motion at the TLSV and increased motion at the disc above the TLSV. There will be a predisposition to DDD.

Schmorls Node
When the nucleus pulposis herniates through the endplate. Can be due to developmental weakness in the endplate, pathological fractures (OP, osteomalacia, trauma). This is not a congenital condition (usually). Radiographic findings: Abrupt, squared rim of sclerosis protrudes the vertebral body. (Looks like you poked your finger into the vertebral body endplate). Usually central or peripheral. Clinical Significance: None.

Congenital Absence of Pedicle (AKA Pedicle Agenesis)

A defect from birth, resulting in the absence of one (right or left) pedicle. Must differentiate from tumor destruction. Radiographic findings: will see a sclerotic contralateral pedicle (which means the defect is congenital). Winking Owl Sign (eyes = pedicles, beak = SP).

Limbus Bone
When the nucleus pulposis herniates through the anterior endplate (secondary growth center). This results in disc material between the vertebrae and the ossicle causing non- union of the secondary growth center. This is similar to a schmorls node. Radiographic Findings: A little bone anterior to the endplate surrounded with smooth cortical bone. Vertebral body height is normal. (You can differentiate this from a fracture because a fracture will not be surrounded with cortical bone on all sides!) Clinical Significance: None. In the picture, the white arrows are pointing to limbus bones, and the yellow arrows are pointing to schmorls nodes.

Para-Auricular Sulci/Para Glenoid Sulci

A completely normal variant caused by pressure erosion from blood vessels. Seen in multi-parous women. Do not confuse this with osteophyte/fracture.

Supracondylar Process
This if found in 1% of Europeans, and it is located on the medial distal shaft of the humerus projecting towards the joint. Do NOT confuse this with an osteochondroma (exostosis), which always points AWAY from the joint.

Coronoid Bone & Os Supratrochlear Dorsale (Joint Mice)

These are small, chronic, post-traumatic osteochondral loose bodies within the coronoid fossa/olecranon fossa, adjacent to the coronoid and trochlear processes. Both are formerly thought to be accessory ossicles. There may or may not be symptoms. NOTE: There is a big difference between ossification and calcification. With ossification, you get the formation of a bone, so it will be corticated. With calcification, you will see NO CORTICES!!! For example, you may see calcification of the supraspinatus tendon under the acromion process, and this will appear as clouds of white on the film where the supraspinatus tendon is located. If you have an unfused secondary ossification center, you will see a corticated piece of bone that looks very regular with smooth margins. So, when you see extra white on a film in the soft tissues, ask yourself if there are cortices, and if there are, call it ossification, and if not, call it calcification.

Knife Clasp Deformity

When L5 SP fuses with the S1 tubercle, creating what looks like a knife. Possibly due to the fusion of the secondary ossification centers of the S1 tubercle to the SP of L5. Radiographic findings: Long SP at L5. Clinical Significance: The megaspinous/long SP of L5-S1 will poke the thecal sac causing pain into the legs.

Transitional Vertebrae
Most commonly at the lumbosacral junction, but also likes the cervicothoracic and thoracolumbar junctions. Do not use the terms lumbarization or sacralization for a transitional vertebra at the lumbosacral junction. Instead term the defect a transitional lumbosacral vertebra (TLSV).

Slipped Capital Femoral Epiphysis (SCFE)

This is a condition that affects young adolescents. You will want to look for Kleins line, and it should transect 1/3 of the femoral head. Once the child is out of the developmental period, you would be worried about fracture.

Spatulated TVPs
Large TVPs that look like spatulas, but only if the TVPs are greater than 19 mm. Can be completely fused with, or can form an accessory joint with the inferior vertebra.

Developmental Dysplasia of the Hip (DDH)

This was formerly called congenital hip dislocations and is detected with the child is born via the dislocation and relocation test. You will want to look for a clunk that means the hip is not sitting in the right place, and occurs from abnormal development. This condition is more common in first-born females and is due to lax soft tissues.

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DDH is characterized by three common things known as Puttis Triad: Shallow acetabulum Superolateral displacement of the proximal femur Delayed ossification of the femoral head (hypoplasic femoral head)

23 sustentaculum tali. If the rear foot is in subtalar neutral at rest, then prognosis is good from conservative care. If the rear foot is everted at rest, then surgical intervention will be needed. Signs of subtalar coalition include the C-Sign, prominent talar beak, a narrow posterior subtalar joint and a ball-and-socket adaptation. Other coalitions include calcaneocuboid and lateral cuneiform-cuboid fusion. These are exceedingly rare, and usually seen with other types of coalition. Conservative treatment should focus on improving joint motion at other joints with manipulation, heating modalities and habilitation. Corticosteroid injections can also help in the acute stage. Surgical treatment: involves resection of the coalition, calcaneal osteotomy and triple arthrodesis. Clinical Significance: the patient will usually have a rigid flatfoot.

When you catch DDH early, it is a good idea to triple diaper the child to stabilize the hip joint and fix this problem.

Os Acetabulae
These are accessory ossicles varying in size or no real significance (which is debatable). DDxs include calcific tendonitis at the capsule or rectus femoris.

Bipartite Patella
This is a common condition caused by an unfused upper-outer quadrant (the patella develops from multiple ossification centers). Do NOT confuse this with a fracture!! All margins will be smooth in bipartite patellas and there will be no soft tissue swelling (unless theres been trauma to the area or something else is going on). Bipartite patellas are bilateral in 60-80% of patients, and is 9 times more common in males. The histological changes in bipartite patellas are identical to those in Osgood-Schlatters disease (tibial tuberosity)/Sinding-Larson-Johannson disease (at the patella). The etiology is likely due to chronic repetitive trauma. It may be symptomatic, and can be seen with an abnormal bone scan. MRI is also helpful to detect stress x-rays.

Persistent Synchondrosis
Includes Types I-III Accessory Navicular bones (Os Tibiale Externa) and Os Trigonum. Type I Accessory Navicular: a 2-3 mm sesamoid bone in the posterior tibial tendon, separate from the navicular and is asymptomatic. Type II Accessory Navicular: is a more triangular ossicle ~1 cm connected to the navicular by cartilage. Persistence of the apophysis for the navicular tubercle. It may be associated with painful pes planus. Type III Accessory (Cornuate) Navicular: is a prominent navicular tubercle, without separate ossicles. It may convert to a Type II as an ununited stress fracture. 80% of asymptomatic Type II convert to Type III but only 20% of symptomatic. Symptoms in Accessory Navicular bones: Type I accessory naviculars are generally asymptomatic, Type II accessory navicular bones commonly have symptoms, and Type III does not typically have symptoms. Bone scans can help to diagnose, and MRIs may demonstrate associated findings. Os Trigonum: is the most common accessory ossicle in the ankle. It is present in 14-25% of adults, and is commonly bilateral. Os Trigonum Syndrome may disrupt the normal chondro-osseous junction, and can result in fracture of the posterior process (which is already fused). This is common in soccer players and ballerinas.

Dorsal Defect of the Patella

This is a condition that affects the upper, outer quadrant of the patella, occurring in 1% of the population and is bilateral in 80% of cases. It is usually asymptomatic. The defect appears as a lucency, and is seen nicely on the PA view.

Tarsal Coalition
This is the congenital fusion of 2 or more tarsal bones, usually the calcaneus with either the talus or navicular. Do not hallucinate this in other bones. Tarsal coalition and unions between bones can have osseous connections, fibrous or cartilaginous. Tarsal coalition can be congenital, surgical, infectious or secondary to an articular disorder. If you see degenerative changes, this is indirect evidence of non-osseous coalition. The most common fusion is calcaneonavicular coalition, which will present with the anteater nose sign. Talocalcaneal fusions are just about as common as calcaneonavicular fusions, but are more commonly symptomatic. The middle facet of the talus fuses with the

24

Talar Beak
This is a common condition involving a process off the distal surface of the talus. It will look like an osteophyte, but it is not close to a joint (look at the medial oblique for this). It can be associated with calcaneonavicular coalition. This is NOT a degenerative phenomenon.

Coronoid Bone and Os Supratrochleare Dorsale

This is a small chronic post traumatic osteochondral loose body lying within the coronoid/olecranon fossa.

Bilateral Madelungs Deformity

This is when there is premature fusion of the medial distal epiphysis of the radius causing a bowing presentation of the radius and causing the distal radius may angulate downwards creating a narrow angle to the carpal bones.

Os Trigonum
This is another common anomaly, and is NOT a fracture. It is the MOST common accessory ossicle in the ankle, and you will see it sitting posteriorly. 14-25% of adults have an os trigonum and it is most common bilateral. It is a condition that involves a tiny os bone or ossicle sitting posterior to the posterior aspect of the talus. There is usually no clinical significance, but can cause impingement (in plantarflexion), especially in sports and ballet dancers, in both the hands and feet.

Terry Thomas Sign

Occurs when there is an increased space between the scaphoid and lunate.

Negative Ulnar Variance

Occurs when the ulna is shorter relative to the radius, possible predisposing the lunate to undergo AVN (Keinbochs Disease) and ulnar impingement syndrome.

Os Trigonum Syndrome
This occurs when the os trigonum presents with an acute or stress fracture with the os trigonum, the patient will likely be a soccer player or ballerina (from all the plantar flexion), and plantar flexion will disrupt the normal chondro-osseous junction, or can result in a fracture of the fused posterior process.

Positive Ulnar Variance

This occurs when the ulna is longer relative to the radius, and is associated with tears of the TFCC (Triangular fibrocartilage) and ulnar impaction syndrome.

Os Intermetatarseum
This is when there is an accessory ossicle between the first and second metatarsals. It is th thought to possibly originate from a vestigial 6 digit, sesamoid bone of developmental variant of the medial cuneiform. May be separate from metatarsal or exist as an exostosis. It is seen in 10% of asymptomatic specimens, but only slightly over 1% of foot x-rays. Clinically, this may result in metatarsus varus leading to hallux valgus.

Os Syloideum

This is an accessory ossicle that is most common at the base of the 2 and 3 metacarpals.

nd

rd

The Normal Apophysis of the 5th Metatarsal

The normal apophysis of the 5 metatarsal is ALWAYS vertical!! Never confuse this apophysis with an avulsion fracture (which is always horizontal). You must determine the skeletal maturity of the patient.
th

Other Os Bones
There are many other ossicles that can occur (in the feet, and elsewhere), and they all have names. Just remember not to confuse them with fractures!!

Bipartite Sesamoids
Sesamoids are on the plantar aspect of the foot underneath the head of the first metatarsal. There are two here, a medial sesamoid and a lateral one. If you see a lucency through one of the sesamoids, then this is a bipartite sesamoid.

Os Acromiale
This is when the acomion has an unfused acromion apophysis.

Supracondylar Process (Humerus)

This will be located along the medial distal humeral shaft of the humerus, projecting towards the joint. NOTE: Osteochondromas point AWAY from a joint!!!! Do NOT get these two conditions confused!! Osteochondromas also have the well known cartilaginous cap!

Club Foot
AKA Talipes Equiovarus, and is a condition characterized by the feet turning inwards. The patient must be braced in order to correct this condition, however if conservative treatment fails, surgery may be required. Club foot is common in first borns due to their position in utero (in a previously unstretched uterus).

Anomalous Feet
This can occur when there are more (supernumery) or less digits.

RADIOLOGY REVIEW

25 rods inserted into the spine. Take lateral flexion views to see if the scoliosis is structural or functional.

Polydactyly
Having more than 5 toes/foot!

Osteopoikilosis
This is a condition that causes spotty bones, and is usually asymptomatic. It occurs in males more than females, and 25% have cutaneous abnormalities. 15-20% have mild joint pain. Osteopoikilosis looks like multiple bone islands, and commonly occurs in the epiphyseal and metaphyseal regions, the long bones, carpals and tarsals.

Achondroplasia
Is the most common type of dwarfism. It is an obvious conditions and clinical diagnosis, not an x-ray diagnosis. This is a hereditary condition, A.D. homozygous = lethal. 90% have normal parents. Radiographic findings: The vertebral bodies are all normal height. In the cervical spine, there is possible basilar invagination. Interpedicular distance stays the same or decreases as you move inferiorly. In the thoracolumbar junction there may be wedging and rounded vertebral bodies (called Bullet Nosed vertebral bodies). In the lumbar spine there will an increased lumbar lordosis causing a horizontally positioned sacrum. Short and wide pedicles in the lumbar spine, as well as mild DJD/DDD can lead to stenosis. L5 sits very low between ilia. There will be posterior scalloping of the vertebral bodies from the pulsating CSF because the spinal canal is small. The pelvic inlet will look like a champagne glass, and the acetabuli will be posteriorly oriented. The femurs will have flared, broad metaphyseal regions, and a 90 femoral neck angle. Clinical Significance: These patients are mentally normal with a normal lifespan, but have a short stature. The short stature is due to shortened extremities, not a shortened spine. The length of the spine is normal however the patients femurs and humerus will be short relative to the forearm and tib/fib with a rolling gait (hip and knee alterations). The patient will present with an exaggerated lumbar lordosis resulting in a protuberant abdomen and prominent buttocks. These patients have unique facial features; they have protuberant cheeks, sunken nasal bridge, and protuberant forehead. Rhizomelia (all bones form from endochondral ossification). Their hands will have short rd th fingers of similar length and a gap between the 3 and 4 digits, called a trident hand. Congenital spinal stenosis can be found in these patients, which can lead to paraplegia (decreased by 50% at L5).

CONDITIONS
Scoliosis
There are two types of scoliosis: Structural and Non-structural/functional. Structural scoliosis is most common, and usually seen in females. It can be congenital, neuromuscular, from neurofibromatosis, or other conditions (infection, radiation). Non- structural/functional can be due to postural problems, leg length inequality, and antalgic gait/position. Radiographic findings: SALAD (Shape, Apex, Location, Angle, Direction). Shape (C or S shaped). Apex (the most deviated segment). Locations (depends on where the apex is, can be cervical, cervirothoracic, mid thoracic, thoracolumbar, lumbar, lumbosacral and double major curves. Angle (measured by the Cobb Angle Method, make lines on the end plates). Direction (determined by the convex side, notice the direction of the arrow- head). Cobb Method for assessing curve: Draw lines along the superior and inferior endplate of the superior most/inferior most vertebrae effected, respectively. Clinical Relevance: A scanogram may be used to evaluate for leg length discrepancy. It takes a radiograph of the hips, knees, and ankles while the patient lies on the table. Other tests may include Adams Test/Forward bending test, the lateral bending test (if the persons curve straightens out, the curve is functional, if the curve doesnt straighten out, this is curve is structural). In recent studies, scoliosis increases the risk of breast cancer. You can help reduce the risk of breast cancer by 50-75% by doing the PA view by the AP view. Management: If the patient is adult, no monitoring is necessary because the curve will not progress. For children, monitoring is necessary. Refer if a child has a 30* curve or more. If a child has a curve of 20-30* screen the child every 3-6 months. If 25-40 degrees, use a brace to halt the progression. If over 50 degrees, surgery with Harrington

Osteogenesis Imperfecta
This is a hereditary disorder (autosomal dominant) of connective tissue affecting the skin, bones, ligaments, tendons, fascia, sclera and teeth, characterized by unusually fragile bones that break easily, often under loads of normal daily stress. There will be an inherent weakness of the bones due to a malfunction in the bodys production of the protein collagen. There are three types of osteogenesis imperfecta. The first is osteogenesis imperfecta congenital, which is rare and very severe. Most of these patients will die at birth because they are born with multiple fractures, have cerebral hemorrhaging and respiratory failure. The second type is osteogenesis imperfecta tarda. This is the most common type of osteogenesis imperfecta, and these patients will have a normal life expectancy. The patient will present with bowing of the bones due to small

 fractures that repair themselves, and other fractures due to trivial trauma. The third type is osteogenesis imperfecta cystica. This is characterized by the femur being driven into the acetabulum. The vertebral bodies will be biconcave and the disc spaces will look fatter than the vertebral bodies. Radiographic Findings: The patient will present with generalized osteopenia (diffuse decrease in bone density) and pencil thin-cortices. The bones will be undergoing bowing, and will have multiple fractures. There are usually flattened vertebral bodies. *There is difference between a deficiency fracture and a stress fracture. Deficiency fractures occur when there are normal stresses on insufficient bone, and a stress fracture is when there are repeated/abnormal stresses placed on normal bone. Clinical Significance: There is a clinical quad for this condition, and in order to diagnose osteogenesis imperfecta, you only need two of the following present: 1. 2. 3. 4. Blue sclera Dentinogenesis imperfecta Osteoporosis Premature hearing loss (beginning in the 20s)

26 Clinical significance: There is variable severity of this condition. If can either be congenital (from childhood) or tarda (from adulthood). The congenital form is more severe, and death often occurs in utero or in the first year of life. In patients will the tarda form, the patient will present with repeated fractures, possible anemia and unexplained bruising.

Osteopoikilosis
This condition looks like polka-dot bones, or bone measles. This condition is a relative of osteopetrosis, and is asymptomatic. You MUST differentiate osteopoikilosis from metastasis. Radiographic findings: Radiopaque oval densities within the ends of long bones, small bones and the acetabulum. Clinical significance: insignificant. This condition is usually discovered incidentally when radiographed for other issues.

Neurofibromatosis
This is also known as Von Recklinghausens Disease. It is seen in 1/3000 births. Neurofibromatosis is a disease of neural and cutaneous fibrous elements leading to skin tumors and nerve sheath tumors. Radiographic findings: Posterior scalloping, dural ectasia (stretching of the thecal sac) and pressure erosions. Kyphoscoliosis (curve in more than one plane) occurs in 50% of cases. Focal giantism can be present and dumbbell tumors. Clinical significance: There is a clinical triad to this condition, which when combined with neurofibromas lead to the diagnosis of neurofibromatosis. 1. 2. 3. Caf au lait spots (pigmented cutaneous lesions), must have 6+ caf au lait spots of 1.5 cm or more in order to diagnose. Various osseous alterations of axial and appendicular skeleton. Cutaneous tumors/fibrous molluscum. Pringles Song: I got neurofibromatosis. What am I gonna do? Cafe Ole spots, fibrum malescum too. Oh NO! I got neurofibromatosis, it's giving me scoliosis! Dural estasia, Posterior scalloping,

Other clinical signs/symptoms include: fragile bones, triangular-shaped face, possible scoliosis, thin and smooth skin, loose joints, low muscle tone and brittle teeth. The patient may have short stature, a barrel shaped ribcage, and possible respiratory problems.

Osteopetrosis
This condition is a rare condition, and is also known as Albers-Schonberg Disease. It is characterized by failure of bone removal during bone turnover, resulting in very dense bones that are very brittle and fracture easily (Dr. Pringle called these very dense bones Marble/chalk bones). To diagnose osteopetrosis, the patient must have : 1. 2. 3. 4. 5. A history of recurrent fractures Compressive neuropathies (narrowed cranial foraminae) Anaemia (decreased bone marrow) Easily bruise (decreased platelets) Splenomegaly (increased organ size in general)

Radiographic findings: Lucency in the middle of the vertebral bodies with increased density around the end plates. There may be pars defects because of the brittleness of the bones. Tubular bones will have little-no medullary cavities, and an Erlenmeyer flask deformity (the femur flares too early in the femoral shaft). The epiphyses of the bones will grow normally, and occasionally alternating bands of sclerotic normal bone at the end of shaft, making it look like there is a bone within a bone.

RADIOLOGY REVIEW
Neurofibromatosis!

27 Radiographic findings: The patient will present with absent/partially absent clavicles. Schisis defects (SBOs) and a wide pubic symphysis. There will be delayed ossification of the cranium and persistent frontanelles and metopic suture. The thorax will often be cone-shaped. Clinical significance: the patient will short, but not quite dwarf stature), with a large head/small face. The shoulders will be dropping, and the thorax will be thin and cone- shaped. The patient will have hip deformities and gait disturbances, with defective dentition (supernumerary teeth). The patient may be able to touch his/her shoulders together.

Pressure Erosions
Dumbbell tumors, Schwannoma/neurilemmoma Focal enlargement of an IVF. Posterior scalloping at one level Possible multiple NOF (non ossifying fibroma) Can cause focal giantism (giantism of one particular part of the body).

Marfans Syndrome
This is a connective tissue disorder caused by a failure to produce normal collagen resulting in lax joints. This condition usually has a familial incidence (autosomal dominant) is most commonly diagnosed clinically. It is caused by a gene mutation for fibrillin (chromosome 15). Fibrillin is an important protein component of blood vessels, eyes, tendons, ligaments and the lungs. Classic signs of weakness in at least two systems (heart, eyes, skeleton) are present. Radiographic Findings: Elongated extremities without increased width of bones, tall vertebral bodies (spool shaped vertebrae) with posterior scalloping (from dural ectasia). There will be a widened spinal canal from increased interpedicular distance. There may be scoliosis, or aneurysms. Long ribs angled downwards are common. Clinical Significance: Symptoms can affect different systems, the skeleton, cardiovascular, eyes and the lungs. The individual may have scoliosis or kyphosis with potentially loose and painful joints. In the cardiovascular system, the individual may suffer from an aortic aneurysm, aortic dissection, or mitral valve prolapse sometimes requiring surgical repair. The eyes can suffer from myopia, dislocation of the ocular lens, retinal detachment or glaucoma. The lungs can have pneomothorax, bronchiectasis or emphysema. The patients will usually be tall and slim. These patients present with joint laxity and easy dislocations that lead to premature DJD. Patient will be able to make the thumb sign, when the patient can tuck his/her thumb into his/her hand and the thumb will stick way out the medial part of the hand. The patients fingers will be very long and spider-like, called arachnodactyly, and very long extremities, with sparse soft tissues and hypotonic musculature. Scoliosis will be present in 45%, lens dislocations in 50%, poor dentition (teeth), and heart disease (33%). Mentally, these patients are normal. There is a predisposition to aneurisms of the thoracic aorta, and must be referred for ultrasound. Dissecting aneurysms of the heart/aorta are a common cause of death. *President Lincoln had Marfans Syndrome!

Downs Syndrome/Trisomy 21
Downs Syndrome occurs in 1/700 births. There are different types of Downs Syndrome: Trisomy 21 (most common, 95%), Translocation 21 (3-4%), and Mosaic 21 (1- 2%). Radiographic Findings: AAI (Atlantoaxial instability) in 15%. Possible scoliosis (50%), commonly in the C/S and T/S, and usually it is a functional scoliosis. Hip subluxations, either partial or complete, where the femoral head moves laterally out of the acetabulum, is common in kids aged 3-13. Legg-Calve Perthes (LCP; AVN of the hip) is slightly more common in kids with Downs. Slipped Capital Femoral Epiphysis is also common (can also be associated with obesity and hypothyroidism). Lateral displacement of the patella (subluxation). Clinical significance: The patient will present with epicanthal folds, oblique palpebral fissures, brachycephaly, and metal retardation. The tongue will be large, and there will be a Simean crease in the hand. Atlanto-axial instability because the transverse ligament can be lax or absent. All children with Downs who want to play aggressive sports should have cervical spine x-rays. When the atlantodental distance is >4.5 mm, restrition of sports is advised. Repeated x-rays are not indicated for children with Downs who have previously had neck x-rays, however AAI can develop in these kids. If the child/adult has atlantoaxial subluxation or dislocation and neurological signs, they should be restricted from all strenuous activities. If the patient has no indication of AAI, the patient may participate in all sports. Most AAIs are asymptomatic, symptomatic AAIs are rare. If the patient has a narrowed neural canal or evidence of marked AAI, the child should have an MRI of the neck before activity restriction or any surgical procedures are done which require anesthesia. Painless limp and loss of full ROM of hip (LVP). Instability of the patella in 20% of Downs, with reduced ROM and altered gait. Patellar instability can progress to dislocation. Pes planus seen in most Downs patients with heavy caluses and an increase in the first ray angle and bone spurs. If mild, the heel will be in neutral position, and if sever, there will be valgus deviation of the heel and the patient will walk on the inside of

Cleidocranial Dysostosis (Dysplasia)

This a condition affecting mainly the intramembranous bones with midline defects. It is an autosomal dominant condition.

 their heel. Metatarsus Primus Varus (distal metatarsal dducts, bunions an dcalluses make it difficult to fit into shoes. There is a higher incidence of joint problems in people with Downs. Not known if JRA is more frequent (Juvenile Rheumatoid Arthritis). Bone density in adults with Downs is lower, with a risk of OP (osteoporosis) in adulthood. Downs children are usually slow moving, enough so that they arent susceptible to injury. Muscles will be hypotonic and may have difficulty moving independently. They may appear floppy or double-jointed. Low muscle tone can cause low tone int eh mouth and tongue, low shoulders, classic upper and lower cross syndrome, poor speech and feeding, delayed gross motor development and skills, and susceptibility to SI dysfunction. Downs children will usually have hypermobility of their joints with diminished proprioceptive sensation, instability which can lead to dislocations (dont life these children from under their arms for fear of GH joint dislocation, lift them from the buttocks or use a buttock strap). Downs children may show postural slumping.

28 Management: Plain film radiography is the least sensitive method for assessing bone quantity and quality. However, it is useful in the initial evaluation. Bone studies are the best.

Osteopenia (Op)
This is a condition known as poverty of bone. It has many causes, including Family History Menopausal/post menopausal/senile Op Alcoholism and Drugs: Corticosteroids, anticonvulsants, and HIV drugs. Lack of Vitamin C, D and sunshine. Malabsorption syndromes: lactose intolerance, gluten intolerance. Pathologies: Liver disease, kidney disease, multiple myeloma, hyperparathyroidism.

Osteoporosis (OP)
This is known as the silent thief, and is an epidemic in our population. It is a disease characterized by reduced bone quantity, and is more common in women than men. Patients will have a hyperkyphosis from multiple compression fractures from weak bones. This can result in Dowagers Hump. There are 3 types of compression fractures: biconcave central compression fractures which occur in the lumbar spine, anterior wedge compression fractures which present in the thoracic spine, and pathological compression fractures, which result in symmetrically transverse vertebral bodies (cake/flat vertebral bodies). Pathological compression fractures can come from metastasis, multiple myeloma, infection, osteoporosis, or eosinophilic granuloma in kids. Radiographic findings: Plain film signs include osteopenia (increased radiolucency of bones), thin cortices, accentuation of weight bearing trabeculae and compression fractures. Keep in mind that all signs are subjective and film quality dependent. *Remember that in the thoracic spine, there is normal anterior wedging of the vertebral body, and the maximum difference allowable in height between the anterior and posterior aspects of a vertebral body is 2-3 mm. You will see Codfish Vertebra where the endplates droop inwards, making the vertebra look like a star, or little xs, or a cod fish. On DEXA, to be diagnosed with OP, you must have a outcome number of <2.5. Op is -1 to -2.5. Normal is >-1. Clinical Significance: 25% of women and 1/8 of men in Canada have OP. In a 50 year old Caucasian women, there is a 40% lifetime risk for developing a hip, vertebral or wrist fracture. The mortality rate is 20% higher one year after a hip fracture. Greater than 50% of women who sustain a hip fracture do not return to their previous functional state. This is a very expensive condition to treat, costing the US $17-20 billion annually. Prevention is key! (CMAJ 2002). When a patient presents with compression fractures at T5 or above, you must consider grand mal seizures at a cause of the compression fracture, as anticonvulsant medication is known to cause osteoporosis.

Liver disease leads to a lack of activation of Vitamin D, and Kidney diseases leads to Op by not activating Vitamin D, and excreting too much calcium. Corticosteroids cause osteoporosis, and can cause osteonecrosis (AVN). Corticosteroids can cause Op when taken from an exogenous source (prednisone), or an endogenous source (Cushings Syndrome, when the adrenal glands do not function and the patient secretes too many corticosteroids). Corticosteroids can cause AVN, and gas containing compression fractures. AVN can also be caused by multiple myeloma, metastasis and radiation necrosis. Radiographic Findings: Generalized osteopenia, can have mini-compression fractures where a limbus bone might be, and it may look bring on film because the body tries to heal the bone fast because of the corticosteroids.

Osteomalacia (OM)
This is when the bones are soft due to poor mineralization, causing reduced bone quality and decreased bone density. OM can be caused by problems with calcium, phosphorus, Vitamin D metabolism, as well as deficiency, malabsorption or renal problems. This condition is commonly asked about on boards. Radiographic findings: Increased lucency of bones, accentuated trabecular pattern, cortical medullary cavity blurring. Pseudofractures. Sign of bone softening (bowing deformities and protrusio acetabuli. You must see signs of bone softening and bowing in order to diagnose OM. Clinical significance: The patient will present with generalized muscle weakness and bone pain on palpation. There is a possibility for possible deformity in weight bearing structures (ex: pelvis, femur, tibia, spine).

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29 GH secreted after skeletal maturity when all bones are fused, then acromegaly will result. Acromegaly is usually caused by an adenoma of the pituitary gland. Radiographic findings: Very thick and protuberant frontal bone, large sella turcica because of tumor growth, EOP (external occipital protuberance) overgrowth from excess bony growth, wide joint spaces initially from soft tissue overgrowth, spaded tufts (the distal end of the distal-most phalangeal bone in the hands begin to look like spades), and overgrowth of the heel pad. The maximum heel pad thickness is 2 cm, if it is any greater than 2 cm, then acromegaly (or obesity) is indicated. This is not an x-ray diagnosis. NOTE: Acro = distal, Mes = middle limb, Rhizo = proximal limb. Clinical significance: The patient will present with a prominent forehead, , malocclusion and broad/large hands/feet from bony overgrowth. Carpal tunnel syndrome, and early DJD may present. The patient may have headaches, and a thick tongue (clumsy speech), along with other soft tissue overgrowth, increased cartilage and fat deposition. Bone spurs can also present. These patients often die from heart disease (among other complications). The patient may be predisposed to early DJD from excess cartilage growth.

Hyperparathyroidism (HPTH)
This is a condition caused by too much parathyroid secretion. The parathyroid (PTH) gland secretes parathyroid hormone, and works by a feedback mechanism. Parathyroid hormone produces osteoclastic activity, drawing calcium from the bones, and decreasing bone density. Parathyroid hormone is secreted with serum calcium is low. (If there is a tumor in any endocrine gland, the gland will usually produce too much hormone). There are three forms of hyperparathyroidism: primary, secondary and tertiary. Primary HPTH is when there is increased PTH from the parathyroid gland itself (because of a tumor in the parathyroid gland, for example). Secondary HPTH is due to renal disease, which leads to calcium loss, therefore increased PTH is secreted to try to increase serum Calcium. Tertiary HPTH is iatrogenic due to dialysis. Radiographic findings: Generalized osteopenia everywhere except at the endplates, resulting in Rugger Jersey Spine. Subperiosteal bone resorption is the diagnostic hallmark (will carve out the bone on the lateral aspects of the phalanges, especially on the second and third digits), acro-osteolysis (when the tips of the distal phalanges are eaten away/separated from the rest of the distal phalange). Brown Tumors (osteoclastoma, a focal area of severe bone loss, making it look like a hole in the bone). Renal Calculi. Chondrocalcinosis (calcification of cartilage) and soft tissue calcifications. Clinical Significance: If the blood calcium levels get too low, the patient can die. History of kidney disease can indicate HPTH.

BONE TUMORS
There are two types of bone tumors: benign and malignant. Benign bone tumors are most common and generally are life-threatening. Malignant tumors are more life- threatening and can be either primary or secondary. Primary malignant tumors are characterized by malignant tumors that start in the bone. Secondary malignant tumors start elsewhere and then spread to the bone. Radiographic findings: In order to see radiographic evidence of bone loss, 30-50% loss of bone density is necessary before it is detectable on radiographs. Location of the lesion: the lesion can occur at different parts of a bone. Lesions can originate in the medullary cavity, in the cortex, or the periosteum. If the lesion starts in the medullary cavity, the lesion will appear central, or slightly eccentric. You may or may not see endosteal scalloping and cortical thinning. If the lesion is based in the cortex, the lesion will be eccentric (but if the lesion is seen en face if may appear to be central, so be sure to check BOTH perpendicular views!). If the lesion is based in the periosteum, there will be littler underlying bone abnormality. Number of lesions: monostotic (one lesion) or polyatomic (multiple lesions).

Cushings Syndrome
This syndrome is due to corticosteroid use. Radiographic findings: Clinical significance: the patient will present with a round/puffy face, with fat pads near the traps, red cheeks, and thin skin. The patient will have a high bruisability and ecchymosis. The patient will have poor muscle development and poor wound healing with lots of adipose tissue around the middle (apple-like shape). There will also be stria on the abdomen (purple-ish stripes).

Acromegaly
This is a condition caused by excess growth hormone (GH) from the pituitary gland. There is one other condition that is also caused by increased secretion of GH, and this is Giantism/Gigantism. The difference between Acromegaly and Giantism depends on when the GH was secreted. If the GH is secreted in excess before skeletal maturity, then Giantism will result; all bones not skeletally mature will get too big. If theres too much

 The matrix of the bone destruction can be fat-based (lipoma), cartilage-based (which will frequently calcifies making it look stippled, flocculent, arc & ring calcifications), osseous-based (will appear ivory) or fibrous (which will have the appearance of ground glass, smokey or hazy). Tumor Characteristic: In order to determine if a tumor is benign or malignant you must determine the tumors behavior, whether it is osteoblastic, osteolytic or mixed. Osteoblastic tumors are bone forming tumors and are whiter, heavier and denser tumors. Osteolytic tumors are bone destroying tumors, and have lighter bone because the bone is being eaten away. Mixed tumors have both a lytic and blastic pattern. Pattern of Bone Destruction: There are different patterns of bone destruction: geographic, moth-eaten or permeative. Geographic patterns of destruction generally indicate a benign lesion, and is when the lesion is clearly demarcated, you will be able to see exactly where the lesion starts and ends and can draw a line around its margins. Moth-eaten patterns of destruction looks like bugs have eaten away at the both, and can be due to either malignancy or infection. Marginization/Zone of Transition: this is the interface between the tumor and the normal bone. The zone of transition can be sharp/short, or poorly defined. If the zone of transition is short/sharp, the lesion is likely benign. If the zone of transition is wide, infection or malignancy is indicated. Cortex: The bone cortex can either be intact, expanded or destroyed. If the cortex is intact, this indicates a more benign lesion. If the cortex is expanded (bulging), the lesion could be benign or malignant. If the cortex is destroyed (eroded/penetrated), the lesion could be benign or malignant. Periosteal Reaction: A characteristic of tumors when calcium is deposited underneath the periosteum. There can be no periosteal reaction, a single layer reaction, laminated/onion skin reaction, codmans triangles or spiculated/sunburst/hair-on-end periosteal reaction. If there is no periosteal reaction, the lesion is benign, or due to metastatic lesions. If there is a single layer of periosteal reaction, the lesion can be benign, infection or traumatic. If there is a laminated/onion skin reaction (a multi- layered reaction), this could indicate infection or primary malignancy. If codmans triangles (the periosteum is lifted away to look like a triangle) are present, the lesion could be infectious or a primary malignancy. If the reaction is spiculated/sunburst/hair- on-end, a primary malignant tumor is indicated. Metastases do not produce periosteal reaction. Note: Codmans triangles: In very malignant tumors (i.e. osteosarcomas), the tumor is so aggressive that it smashes through the cortex, and ventures out of the bone and into the soft tissues. This raises the periosteum of the bone, creating the Codmans Triangle.

30 Soft tissue mass: Soft tissue mass may or may not be present. If there is a soft tissue mass, the lesion is likely primary malignant. If there is no soft tissue mass, the lesion is likely benign or metastatic. Symmetry: symmetry is usually due to disseminated diseases that interfere with bone function and metabolism (such as HPTH, osteomalacia, OP, leukemia). Things you need to consider: Clinical data/History (age, pain, length of time with complaint) Number of lesions Description of the lesion Behavior of the lesion Matrix of the lesion Margination Cortical involvement Periosteal reaction Soft tissue involvement Joint involvement Further imaging/management o Think of describing lesions from the inside out

Tumors do not like to cross joints, but infection does! Radiographic findings of benign bone lesions: Well, defined, short zone of transition with sclerotic borders, no periosteal reaction, no soft tissue mass, not painful. Clinical significance: Note the age and sex of the patient. Find out the history of the lesion, was there trauma? Is there pain? Swelling? Fever? Is there a history of cancer? Etc. As a general rule, benign bone tumors are not painful. However there are three exceptions that do cause pain; osteoid osteomas. Chondroblastomas, and Aneurysmal Bone Cysts all cause pain. Bone Tumors can be classifed as follows: Hematopoietic: (40%) Myeloma, malignant lymphoma Chondrogenic (22%) Osteochondroma, chondroma, chondroblastoma, chondromyxoid fibroma, chondrosarcoma. Osteogenic (19%) osteoid osteoma, osteoblastoma, osteosarcoma. Unknown origin (10%) giant cell tumor, ewing tumor, adamantinoma. Histiocytic origin Fibrous histiocytoma, MFH. Fibrogenic Metaphyseal fibrous defect (fibroma), desmoplastic fibroma, fibrosarcoma. Notochordal Chordoma.

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31 Clinical significance: The patient will usually present with painless and lumpy joints. There may be growth deformities because osteochondromas usually arise out of the growth centers (metaphyseal region). There is a high rate of malignant degeneration with HME! Management: Refer if there is pain of swelling. Enostoma/Bone Island This is an asymptomatic lesion presenting radiographically as a solitary sclerotic lesion/focus of cortical bone in the medullary cavity. It is common in the ischium and illium, sacrum, and proximal femur, but can present anywhere except the skull, and never in the diaphysis of a long bone. Differential diagnosis includes blastic metastasis in the elderly. Dr. Pringle described bone islands as patchy, cortical bone where cortical bone shouldnt be. Differential diagnoses include blastic metastasis and an osteoid osteoma. Radiographic findings: a round, solitary, sclerotic lesion, which may have a brush border appearance. Usually found in the epiphysis or metaphysis. On a bone scan, the lesion can appear as warm. Clinical significance: Enostomas are asymptomatic. There is no potential for malignant degeneration. However, the lesion may or may not grow in size.

Benign Osseous Lesions

The benign osseous lesions include: Osteochondroma (Pedunculated/Sessile) HME (Hereditary Multiple Exostosis) Enostoma (Bone Island) Osteoid Osteoma (OO) Osteoblastoma (Giant OO)

Osteochondroma This is the most common benign skeletal tumor, and is usually found in the metaphyseal regions of the extremity. Osteochondromas can also be called cauliflower exostosis. Osteochondromas are a bony exostosis with a cartilaginous cap that projects away from bone. There are two types: pedunculated and sessile. Pedunculated looks like a stalk of broccoli, where the base is the bony part, and the flowery part of the cauliflower is the cartilaginous cap. Pedunculated osteochondromas are common in the hip, knee and ankle. Sessile osteochondromas just look like a broad base with no stalk, commonly in the humerus and scapula, and can occur in the spine. They usually appear in 10-30 year old patients, and is autosomal dominant inherited. It is common in kids and there is thought that it arises from a disruption of the growth plates.

Radiographic findings: Bony outgrowth (exostosis) from the cortex of the metaphysis of long bones with either a broad (sessile) or narrow (pedunculated) base, that projects Osteoid Osteoma (OO) away from the bone, and towards the joint. The cartilage cap has stippled calcifications. This is a painful lesion with a lucent central nidus and a sclerotic border, that is worse at night and relieved with aspirin (ASA). It is most commonly located in the medial part of Clinical significance: Usually asymptomatic, unless the lesion has been fractured, or the femur, and likes to present in 10-25 year olds, with a 2:1 M:F predominance. It loves interferes with vessels or nerves. Usually will present as a painless hard mass near a the appendicular skeleton. If found in the spine, it will target the posterior arch (rigid, joint. Other complications include pain from spontaneous enlargement or pain from a painful scoliosis). Reactive sclerosis (alpha-sclerotic pedicle). Differential diagnoses fractured stalk, neural encroachment or irritation, irritated bursa over cap or malignancy include Brodies abscess (the nidus is >1 cm). (1%). Should not grow further than skeletal maturity. Most occur (75%) before the age of 20, more commonly in males. This is a normal condition in childhood, however if it Radiographic findings: A lucent lesion (nidus) with a ring of reactive sclerosis surrounding grows in adulthood, it could develop into a chondrocarcoma. it, usually < 1 cm in diameter on a radiograph. The lesion can be intramedullary or Management: No treatment necessary in most cases. If the lesion is symptomatic and large enough, it can be treated by surgical excision. This lesion can undergo malignant degeneration. Hereditary Multiple Exostosis (HME) HME is an inherited disease usually discovered in childhood. It is characterized by multiple bony exostosis through the body (usually about 10 exostoses). HME is basically the presence of many osteochondromas. Radiographic findings: multiple bony exostosis. subperiosteal. Clinical significance: The patient will present with severe pain, especially at night and relieved by aspirin (ASA). If the lesion is near a joint, there may be an arthritis response. Muscle atrophy may be present, limb deformity, and scoliosis if the lesion is in the spine. There is no malignant potential with OOs. *Osteoid Osteomas are an exception to the rule that benign tumors are painless! The only other exception is chondroblastoma. Management: To confirm your diagnosis, send the patient for a bone scan. After diagnosed, refer the patient to a GP, as the nidus needs to be surgically removed. If the

 OO is in the vertebral body, it is often treated with irradiation. Chance of recurrence is rare. Osteoblastoma/Osteoid Blastoma This is a rare bone tumor, usually occurring in the spine (the neural arch, TVP, SP and laminae). It usually presents in patients aged 10-20 YOA, but 70% of the time it occurs before the age of 20. Histologically, this is a giant, more expansile osteoid osteoma! Radiographic findings: Unilateral sclerotic pedicle. On the AP view, there will an expansile, lucent mass around the vertebral body. Expansile lesion with a nidus >2 cm that loves the neural arch. If osteoblastomas are found in tubular bones, there is no reactive sclerosis. Clinical significance: Patient will present with localized dull pain that is worse at night, however the pain is less severe than the pain associated with an osteoid osteoma. The pain is not relieved by aspirin. Management: This condition requires referral for surgical curettage/ simple excision. Spinal lesions are often incurable and require radiation therapy.

32 where an enchondroma has been diagnosed, the lesion could progress to chondrosarcoma. Olliers Disease (Multiple Enchondromatosis) This is very similar to an enchondroma, but instead of there only being one lesion, there are many lesions (hence the name, multiple enchondromatosis = an abnormal condition involving multiple enchondromas). Radiographic findings: Expansile lesions with stippled calcifications, that may even look soap bubbly. Clinical significance: The most common risk of malignant degeneration from Olliers is when the lesion presents in the pelvis and shoulder. Risk of malignant degeneration is typically rare. As a general rule, when you have multiples of any lesion, of the lesion is located closer to the axial skeleton, the risk of malignant degeneration increases. Maffuccis Syndrome This is a rare condition that is very similar to enchodromas, except there will be associated soft tissue hemangiomas associated with the enchondromas. Radiographic findings: The radiographic findings will be identical to enchondromas, except there will also be soft tissue hemangiomas. Clinical significance: There is a greater chance of malignant degeneration than enchondromas, along with ovarian carcinomas and brain gliomas. Chondroblastoma (Codmans Tumor) *GET MORE INFO FROM Y&R Chondrobastomas is a painful tumor that presents in 10-25 year olds. Radiographic findings: Lesion occurring in the epiphysis or apophysis of the knee, hip or shoulder. Clinical significance: This is the second exception to the rule that benign tumors are not painful, because Chondroblastomas are painful. Chondrobastomas may also cause swelling. *If the patient presents with these signs/symptoms and the patient is under 20 years of age, think chondroblastoma. If the patient is over 20, think GCT.

Benign Cartilaginous Lesions

The benign cartilaginous lesions include: Enchondroma Olliers Disease (Multiple Enchondromatosis) Maffuccis Syndrome Chondroblastoma (Codmans Tumor)

Enchondroma This is the most common benign tumor of the hands and the feet. It is founds in 10-40 year old patients. Enchondromas are found in bones that have been preformed with cartilage. Differential diagnoses for enchondromas include bone infarcts if it is found in large, tubular bones. They are usually found in the matphysis of tubular bones, are usually under 3 cm. They appear gray-blue, translucent with a nodular configuration. Radiographic findings: There will be a radiolucent lesion with stippled calcifications within. It is a well defined lesion with no sclerosis, usually found in the medulla of the metaphysis. The lesion will be well-circumscribed and oval, surrounded by a thin rim of radiodense bone, called the O-Ring Sign. Clinical significance: If the patient has had a long history of corticosteroid use, this may point you to enchondroma. The patient will present with not pain (unless the lesion has fractured). If the patient is experiencing pain, refer them to their MD. Malignant degeneration of enchondromas is rare, but if the patient is experiencing pain in a place

Benign Fibrous Lesions

Benign fibrous lesions include: Fibrous Xanthoma (FCD, NOF) Fibrous Dysplasia McCune Albright Syndrome

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Fibrous Xanthoma (Non-Ossifying Fibromas & Fibrous Cortical Defects) Fibrous Xanthomas are a focal growth disturbance (and are not really a true tumor). There are two types of fibrous xanthomas. The first are non-ossifying fibromas (NOF), and the second are fibrous cortical defects (FCD). Fibrous xanthomas usually occur in children 4-8 years of age with FCDs, and a little older with NOFs (8-20 years of age). *FCDs are smaller in size and are in smaller people, NOFs are bigger and are in bigger people. Radiographic findings: These are cortical, lytic, soap-bubbly lesions in the diaphysis or metaphyseal region (But usually always in the metaphysis of long bones). NOFs love the distal femur or tibia, but can also be found in the upper extremities. If the lesion is less than 3 cm, the lesion is likely a FCD. If the lesion is greater than 3 cm, it is likely a NOF. Clinical significance: The patient will usually have no symptoms unless the lesion pathologically fractures. There is no malignant potential. Usually, fibrous xanthomas go away on their own. If treatment is required, surgical treatment with bone grafts can be cone. Differentials for a NOF include: Chondromyxoid Fibroma and ABC. Chondromyxoid fibroma will have the same distribution and presentation as a NOF, but it less common and consists of cartilage. Chondrymyxoid fibroms usually arise in the metaphysis of long bones, and patients usually complain of localized dull, achy pain. The tumor is well circumscribed, solid, tan-grey color, and 3-8 cm big. ABCs are destructive, expansile and dilated tumor-like osseous lesions with a proliferation of connective tissue with multiple blood-filled cavities. Fibrous Dysplasia (FD) This is an asymptomatic condition, commonly known as the great mimic, because it can mimic almost anything. Remember that Pagets is also a great mimic. Fibrous dysplasia is a developmental disturbance in cancellous bone maintenance, with fibrous tissue replacing bone tissue. FD usually appears in late childhood (8-14), and is rarely seen in the spine. There are three forms of FD: Monostotic (solitary lesion, most commonly seen), Polyostotic (FD seen in multiple bones), and McCune-Albright Syndrome (a polyostotic fibrous dysplasia associated with skin pigmentation and precocious sexual development). McCune Albright syndrome is the most rarely seen form of FD. Fibrous dysplasia occurs in a bone when it undergoes physiological resorption and replacement with abnormal proliferation of fibrous tissue. Radiographic findings: There will be a thick rim (indicating a long standing lesion) of cortex around the core with a lucency on the inside that has a ground glass/smokey appearance. There will be associated bone expansion, widening of the medullary cavity, endosteal thinning, and scalloping. Shepherds crook deformity of the femur is common. If the lesion is polyostotic, the lesion prefers to stay on one side of the body. Bowing deformities are common, pathological fractures, Cherubism (familial fibrous dysplasia of the jaws), and leontiasis ossea (overgrowth of the facial bones).

33 Clinical significance: Fibrous dysplasia commonly presents with caf au lait spots (however the spots will have rougher borders than in neurofibromatosis). In Monostotic FD, deformities are rare, and the monostotic form will not progress into the polyostotic form (FD does not spread). In McCune Albright Syndrome, there is a clinical triad of signs and symptoms that will present: (1) Polyostotic fibrous dysplasia, (2) Caf au Lait Spots, (3) precocious puberty. McCune Albright Syndrome McCune Albright Syndrome is polyostotic fibrous dysplasia (multiple lesions of fibrous dysplasia) with caf au lait spots and precocious puberty. Radiographic findings: Identical to fibrous dysplasia except there will be multiple lesions. Clinical significance: Caf au lait spots and precocious puberty.

Benign Cystic Bone Lesions

These are the benign cystic lesions: Simple Bone Cyst (SBC) Aneurysmal Bone Cyst (ABC)

Simple Bone Cyst (SBC) Simple bone cysts are a growth disturbance creating a fluid-filled lesion usually presenting in 8-14 year olds. SBCs arent true tumors either. Radiographic findings: SBCs usually appear in the humerus and proximal femur. They are central lesions, occurring in the metaphysis that usually do not expand more than the growth plate itself. The lesion is radiolucent and trabeculated with a soap bubbly appearance. If the tumor pathologically fractures, the fallen fragment sign should be seen. Aneurysmal Bone Cyst (ABC) This is a big cyst that replaces bone with a proliferation of the vascular component of bone marrow. ABCs can be primary (tumor) or secondary (from trauma). It targets patients 5-20 YOA, and loves the neural arch. This is the only benign tumor known to cross the epiphyseal plate. Differential diagnoses include osteoblastoma. Radiographic findings: Grossly expansile, lytic lesion with fine trabeculation and well defined margins occurring in the cortical bone of the metaphysis (maybe in the diaphysis and medullary cavity). The lesion will have a ballooned-out appearance (commonly known as the finger in balloon sign, which is a term commonly used when an ABC targets the posterior arch of the spine). Also loves the neural arch, but is also found in long bones.

 On CT, an ABC looks massive and bubbly. On MRI you will see higher fluid levels. In long bones, the lesion is eccentric, metaphyseal and a saccular protrusion. *To differentiate and ABC from an Osteoblastoma, know that ABCs are usually more expansile and dont usually present as radiopaque lesions, whereas osteoblastoma can appear radiopaque.

34 Clinical significance: clinically silent, with no malignant potential. Osteoma This is an asymptomatic and benign bone tumor that arises from the intramembranous bones. It likes to be in the frontal and ethmoid sinuses, and the inner and outer tables of the skull.

Clinical significance: Patients will present with relatively acute pain at the site of the lesion, and usually with a history of trauma. ABCs are more common than osteoblastomas. This is the third exception to the rule that benign tumors are painless. Radiographic findings: A round/oval, well circumscribed and radiopaque structure that is usually not bigger than 2 cm. A giant osteoma can cause expansion of the sinus walls. In Management: Refer these patients out for removal of the lesion. Surgical curettage can intramembranous bones, it will be homogenously opaque (the sinuses, mandible, and be used, replacement bone chip therapy or radiation therapy if the lesion is inoperable skull bones). (i.e. in the spine). Patients have a 50% chance of recurrence. Clincal significance: An osteoma rarely obstructs sinus drainage, and has no malignant potential. Miscellaneous Benign Bone Tumors There are two miscellaneous benign bone tumors: Intraosseous lipoma Hemangioma Osteoma Management: if the osteoma is symptomatic, surgical excursion is suggested. Otherwise, no treatment is necessary.

Primary Quasi-Malignant Bone Tumors

There is only one quasi malignant bone tumor, which happens to be 20% malignant and 80% benign: Giant Cell Tumor

Intraosseous Lipoma This is a lipid-based lesion that is similar to a soft tissue lipoma. Intraosseous lipomas are the more rare type of primary bone tumor. Radiographic findings: Lucent lesion with calcification throughout. Commonly found in the calcaneous. Clinical significance: Usually, the patient is asymptomatic. Hemangioma This is the most common benign tumor of the spine caused by newly formed capillary, cavernous and venous blood vessels. This condition develops after puberty and is usually solitary. Hemangiomas love the spine and the skull. Usually seen in patients over 40 years of age. This is the tops and bottoms tumor. There are two types of hemangiomas: capillary and cavernous. Capillary hemangioma is characterized by find capillary loops that spread out, whereas cavernous hemangioma has larger, thin walled vessels with sinuses. Cavernous hemangiomas are more common than capillary hemangiomas. Hemangiomas can occur in osseous and soft tissue structures. Radiographic findings: Vertical striations in the vertebral bodies (corduroy cloth appearance). On CT there will be striations in the transverse plain, seen end on. When looking at a view of the skull, there will look like there are holes in the skull with a central focus in the middle with spokes radiating out. Rarely linked with stenosis. *Can occur anywhere in the bone.

Giant Cell Tumor (GCT) This is the quasi-malignant tumor, and occurs in 20-40 year old patients. They are characterized by the presence of multinucleated giant cells (osteoclast-like). This is a benign tumor with unpredictable behavior. It usually affects the long bones in skeletally mature individuals. They are usually eccentric and arise in the epiphysis and metaphysis of long bones, and extend toward the articular surface. This is a radiolucent lesion, and is destructive in nature with a narrow zone of transition and no surrounding sclerosis. It is purely destructive, there is no bone formation (this differentiates GCTs from Osteosarcomas!). There is no periosteal reaction and no soft tissue masses (unless a fracture has occurred). GCTs have a classic soap-bubbly appearance. Radiographic findings: GCTs always start metaphyseal, but can extend into the subchondral joint space (epiphysis). The GCTs lesions are greatly expansile lucent, soap bubbly lesions with well-defined, not sclerotic borders. GCTs are commonly found in the sacrum. The lesion will often times expand the bone, but will not invade the cartilage. This is a common characteristic of GCTs. Clinical significance: The patient will present with localized, achy joint pain (since the lesion grows towards the growth plate and can destroy that joint) and swelling. *If the patient presents with these signs/symptoms and the patient is under 20 years of age, think chondroblastoma. If the patient is over 20, think GCT.

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nd Differentials: Metastasis (2 differential because these are common in the femoral head of older patients), fibrosarcoma, malignant fibrous histiocytoma, and an ABC. Osteosarcoma is not included because it is bone forming, GCTs are not (however they both are destructive ahd contain multinucleated giant cells.

35 Parosteal Osteosarcoma This lesion occurs in 30-40 years of age, and is an osteosarcoma arising adjacent to the cortex. This is a very rare tumor, and they are generally lower grade than osteosarcomas in general, and create no periosteal reaction. They rarely invade the bone, and have a cartilage cap in 30% of cases. There are two types of osteosarcoma, on osteosarcoma coming right from the bone, or a parosteal osteosarcoma which comes from the periosteum and the surrounding soft tissues. The osteosarcom arising from the bone (see above) is more aggressive and malignant, whereas the periosteal version is less deadly, low grade and has a better prognosis. Radiographic findings: This is an extraosseous sclerotic lesion with a greater density centrally. The lesion is connected to the parent bone by either a broad base (sessile) or a stalk (pedunculated). These lesions occur in the metaphysis. *The epicenter of the lesion is external to the bone. Clinical significance: The patient will appear with dull, intermittent pain. Differentials include: osteochondroma, myositis ossificans, surface osteosarcoma, dedifferentiated parosteal osteosarcoma, high grade surface osteosarcoma, or periosteal osteosarcoma.

Osseous Malignant Bone Tumors

These are the osseous malignant bone tumors: Osteosarcoma Parosteal osteosarcoma

Osteosarcoma Osteosarcomas are the second most common primary malignant bone tumor that typically occurs in 10-30 year olds. There are 5 types, but the central type is the most common. Osteosarcomas are most common in the distal femur and proximal tibia, with accompanying soft tissue masses. The knee is the most common location (60%), followed by the pelvis/hip (15%), shoulder (10%), and face (8%). Bone or osteoid matrix produced by the tumor cells is necessary for diagnosis (pathologically). This tumor is the only one that produces BONE TISSUE, although there are many subtypes of osteosarcoma where osteoid tissue is produced along with other tissues, they are still classified as an osteosarcoma because bone tissue had been produced. Other tissues may be produced, but as long as there is osteod tissue present, it can be classified as osteosarcoma. For example, there are many different types of ostesarcomas, including: osteoblastic, chondroblastic, fibroblastic, MFH-like, Giant cell rich, small cell, epithelioid, telangiectactic, and low-grade central. Radiographic findings: Osteosarcomas appear as lucent lesions with ill-defined lesions. It will have permeative to moth eaten bone destruction, with spiculated or laminated periosteal reaction. This is a cortical lesion that likes the metaphysis, possibly in the diaphysis and medullary cavity. There will be cortical destruction and a soft tissue mass. Rarely found in the spine. Clinical significance: The patient will present with insidious onset of intermittent pain and swelling, and there is usually a history of trauma. The five-year survival rate is 20%, however with chemotherapy and amputation this percentage has increased to 80%. Osteosarcomas usually metastasize to the lungs, liver and skeletal system. Pulmonary metastases is seen in 10-20%. Treatment usually involves chemotherapy followed by resection (limb-sparing) and post-op chemotherapy. They stopped doing amputations on these patients because they found that even though they remove the limb, the risk of metastasis didnt improve. Chemotherapy and radiation is now preferred, along with excision.

Cartilaginous Malignant Bone Tumors

There is only one cartilaginous malignant bone tumor: Chondrosarcoma

Chondrosarcoma Chondrosarcomas are the third most common primary malignant bone tumor. It is a cartilage based bone tumor, so the tumor is entirely hyaline cartilage (with no bone formation otherwise it would be classified as an osteosarcoma). They can be primary or secondary (from a benign lesion), and usually present in patients 40-60 years of age. Chondrosarcomas tend to like the trunk and pelvis, and present with dull aching pain that often wakes the patient at night. Chondrosarcomas are lobulated with loosely arranged chondrocytes. Endochondral ossification often occurs with this type of tumor. Dr. Saad says that this is really the only tumor that we will see in the old population, and its usually found in the pelvis. Note about night pain: pain is caused by inflammatory mediators. During the day, the patient will be moving around and there will be good blood flow and cirulation throughout the body, hence the mediators will be constantly flowing throughout the body. When the patient goes to sleep, circulation decreases and becomes stagnant and the mediators will settle and cause more inflammation and thus more pain. Radiographic findings: Radiolucent lesion with arc and ring calcifications usually occurring in the metaphysis of long bones, in the pelvis or vertebral body. There will be ill-defined margins with endosteal scalloping.

 Clinical significance: The patient will present with dull, aching pain, with or without swelling. If the patient is experiencing persistent pain in a previously diagnosed enchondroma, the pain could be from undergoing malignant degeneration of the enchondroma to chondrosarcoma. These lesions are difficult to treat, so surgery is the primary treatment choice. Low grade lesions receive surgical curettage (scrape/scoop it out) and bone grafting, sometimes with adjunctive techniques. Large low grade or high grade lesions are resected completely.

36 collapse. *To help differentiate between lytic mets: lytic metastasis does not like to appear in the mandible. Clinical significance: The patient will present with localized pain and normal laboratory findings. Solitary plasmacytomas are malignant lesions, and 70% of these patients will continue on to have full-blown multiple myeloma. 90% of patients with solitary plasmacytoma patients die within three years, similar to MM. Multiple Myeloma (MM) This is the most common primary malignant bone tumor. Most patients with MM are between the ages of 50-70 YOA (rarely affects younger patients), and affects males more than females (2:1). Multiple Myeloma occurs when normal marrow is replaced by malignant proliferation of the plasma cells (resulting in weak bone). Differential diagnoses for multiple myeloma include lymphoma (which doesnt typically affect older patients like this), lytic metastasis (this will not have relief with rest). *To remember this DDx list: Multiple myeloma, lymphoma and mets. MM loves the axillary skeleton (red marrow sites), and the lumbar and lower thoracic spine. Radiographic findings: Generalized osteopenia (cortical bone destruction and radiolucent bones). There will be multiple, geographic, well-marginated osteolytic defects (punched out lytic lesions). MM likes to appear in the diaphysis of long bones, and in the vertebral bodies (but it spares the pedicles). May see pathological and/or compression fractures. Rain-drop skull may be present (many little uniform shaped holes in the skull, which can be different skulls, looks like little rain drops falling on your head and burning holes into the skull). Paravertebral soft tissue stripe will be seen. Multiple myeloma is often normal or even cold on bone scans because the bone scan picks up high metabolic/osteoblasic activity, but MM is osteolytic with low metabolic activity. MRI is highly sensitive to marrow infiltration, so will pick up MM nicely. This is NOT a film diagnosis, you will need a biopsy/blood work. *Dr. Pringle started singing Rain drops keep falling on my skull. *Compression fractures will not destroy the IVDs, pathological fractures will. *Multiple myeloma does not like to destroy the posterior elements without taking the vertebral body first. Clinical significance: The patient will appear with insidious onset of pain which progresses in severity, and will often imitate musculoskeletal pain which is worse with activity and better with rest. The patient will often have anemia (very fatigued), will bruise easily and get infections easily. The patient may also have renal disease. Laboratory findings: Anemia, leucopenia, thrombocytopenia, hypercalcemia, hyperuricemia, elevated ESR, and abnormal protein electrophoresis (albumin and globulins, one type of gamma-globulin will be very elevated, mono-globulin spike). Bence Jones Proteinuria.

Fibrous Malignant Bone Tumors

There is one fibrous malignant bone tumor: Fibrosarcoma

Fibrosarcoma Fibrosarcomas can be either primary or secondary (from Pagets, or Fibrous Dysplasia). Radiographic findings: This is a 100% lytic lesion with a huge soft tissue mass. They love to appear in the knee (Lichtensteins Rule), and rarely present with periosteal reaction. Clinical significance: Patients with fibrosarcoma will present with pain and swelling. There is a risk of pathological fracture, and the five-year survival rate is 30%.

Round Cell Malignant Bone Tumors

These are the round cell malignant bone tumors: Solitary Plasmacytoma Multiple Myeloma Ewings Sarcoma Hodgkins Lymphoma Non-Hodgkins Lymphoma Synovial Sarcoma Adamantinoma

Solitary Plasmacytoma This condition a single focus of plasmocyte proliferation in one spot. It is very similar to MM, the only difference is the number of lesions. Solitary plasmacytomas are less common than multiple myeloma, and 50% of cases present before the age of 50. Radiologic findings: A solitary plasmacytoma is a geographic, lytic, expansile, and often soap-bubbly lesion that loves to present in the mandible, ilium, vertebrae, ribs, proximal femur and scapula (the axial skeleton). You may see an increased density due to bone

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Management: Refer out! This patient will need high doses of chemotherapy and stem- cell transplantation (current treatment of choice). Two studies showed an increased survival of one year over chemotherapy alone. Bisphosphonates are routinely given to improve the bone density and reduce skeletal complications. Solitary plasmacytomas are treated with radiation therapy and surgical excision. Survival up to one decade after diagnosis is rare, 90% die within 3 years. Ewings Sarcoma Ewings sarcoma is a malignant round-cell tumor which accounts for 6-10% of primary malignant bone tumors. It is a rare disease where cancer cells are found in the bone/soft tissue. I loves to present in the pelvis, femur, humerus, ribs and clavicle. They commonly arise from the medullary cavity, and are most common in young male teenagers. It likes to present in children to young adults. Ewings is the fourth most common primary malignant bone tumor, and is the most common tumor to produce metastasis to other osseous sites. Radiographic findings: A lucent lesion with permeative bone destruction and ill-defined margins, and laminated or spiculated periosteal reaction. It likes to occur in the diaphyseal region of long bones. Clinical significance: The patient will present with local pain, a soft tissue mass and swelling. Ewings sarcoma often simulates an infection. There is a 35% five-year survival rate. Ewings is the most common tumor to metastasize to other osseous sites. Translocation t(11;22) (q24;a12) is a key diagnostic factor, it is found in 85% of patients. Hodgkins Lymphoma (HL) There are two types of lymphomas: Hodgkin Lymphoma (HL) and Non-Hodgkins Lymphoma (NHL). HL is a disease that usually presents secondary to systemic diseases, often originating in the lymphatic tissues of the chest, liver, spleen and nodes. When HL present in the bone, it targets the vertebral bodies (innominate, scapula, sternum, and ribs (axial skeleton)). It likes younger patients, especially in the 20-30 age range. Differential diagnosis for HL includes blastic mets. Radiographic findings: Most HL lesions are lytic (75%), and only 15% are sclerotic (HL is in the differential list for an ivory vertebra). 10% of HL lesions are mixed with a periosteal reaction. In 2/3 of patients, there will be more than one lesions (polyostotic). Rarely seen anterior vertebral scalloping due to pressure erosions from enlarged lymph nodes. *Pre-sacral soft tissue space should be no more than 2 cm. HL loves the vertebral bodes, especially in the lower thoracics and upper lumbar vertebrae, otherwise it will appear in the diaphysis of long bones.

37 Clinical significance: The patient will present with pain and neurological signs if there is vertebral body collapse. There is a 10-80% five-year survival rate. The osteolytic presentation of HL is more symptomatic than mixed/blastic forms. Management: These patients need immediate referral for radiation and chemotherapy. Five year survival rates are only 10%, but with early detection and effective treatment, five year survival rate can be as high as 80%. Non-Hodgkins Lymphoma (NHL) NHL doesnt stand for the National Hockey League in this case it stands for Non- Hodgkins Lymphoma. It is also known as Reticulum Sarcoma of Bone, and is again usually secondary to systemic disease, and is the primary lymphoma of bone. It presents as localized a solitary lesion in bone, with similar distribution to Hodgkins (spine, pelvis, sacrum, clivus and long bones). NHL also likes C2. It occurs in all age groups, but peaks later on in life, especially from 45-65 years of age (Y&R says 20-40 YOA). Radiographic findings: Lytic destruction in the medullary space of the diaphysis or metaphysis of long tubular bones. There is moth eaten to permeative bone destruction, and laminated/solid periosteal reaction. NHL loves the vertebral body and diaphyses of long bones. Pathological fractures occur in NHL more than any other primary malignant bone tumor. Soft tissue masses are common, and 50% show amorphous calcification. Clinical significance: The patient will present as either asymptomatic or with dull, aching, localized, intermittent pain that is not relieved by rest, however otherwise, the patient will be strikingly healthy. 50% of signs and symptoms for over one year. The five-year survival rate is 48%. Management: These patients must be referred for radiation therapy and chemotherapy. Five year survival rate is 48%. Synovial Sarcoma This is the only primary malignancy that is directly related to a bones surface! It can occur in the tendon sheaths. Clinical significance: this lesion must be surgically removed. Adamantinoma This lesion is not well understood. There are only 150 cases, and almost all cases were reported in the tibia. Management: Amputation.

Miscellaneous Tumors
There is one miscellaneous tumor we looked at:

 Chordoma Chordoma This a very rare tumor arising from notochordal remnants. There are only about 1000 cases reported. It is largely aggressive with a very slow growth rate. It is very tough to get at surgically, and does not usually metastasize. It loves the ends of the skeleton (Tops & Tails). Chordomas also like C2, but can occur in the spheno-occipital region, the clivus and the vertebral body. Radiographic findings: There will be lytic destruction and a soft tissue mass in the sacral base and skull area. Clinical significance: There is a poor prognosis, 3-5 years typically for the different types of chordomas. Management: This patient requires referral for radiation therapy, and resection.

38 two when they present in the spine because multiple myeloma does not like to destroy the posterior elements without taking the vertebral body first. Lytic mets, on the other hand will take anything and everything. Blastic mets can originate from prostate cancer (PSA and acid phosphatase), breast cancer, lung, pancreas, bladder and colon cancers. You will see increased alkaline phosphatase (osteoblasts) with blastic mets. Diagnosis of metastasis is often first made by radiographic findings and lack of physical findings. *Active bone marrow decreases in older patients, but in smokers, the fatty bone marrow decreases and active bone marrow increases. How do you decide if a lesion is a primary lesion or a secondary lesion (metastasis)? It depends on a lot of factors such as the patients age, if the patient has history of previous cancer, and location of the lesion. With a primary malignancy, the lesion will be at one site (usually) and bone tumors dont like to metastasize to bone. So it is most likely that if you see a bone tumor, it is a primary, or a secondary from a visceral tumor. If you see lesions in multiple bones, think metastasis. Radiographic findings: Lytic/blastic or mixed lesion. Blown out metastasis appear as bubbly, expansile and lytic lesions. Winking Owl Sign (with no contralateral sclerotic pedicle, which would indicate pedicle agenesis). *Tumors do not like to cross joints (infections and degeneration does). *if you see the winking owl sign, look for other missing structures (TVP, rib, lamina). *30-50% of bone destruction is needed to be seen on plain films. Bone scans are good for picking up metastatic lesions. There is no periosteal reaction with metastasis, however there is only one exception, and this is blown out metastasis, which can have periosteal reaction. There is also another general rule, which is that metastasis dont have soft tissue mass associated with them, however, blown out metastasis is again an exception because it can produce a soft tissue mass. Metastasis like the axial skeleton, proximal femur, and humerus, in descending order of frequency. MRI is the most sensitive and specific imaging modality to detect early osseous metastasis. Lytic mets have low signal intensity on T1 weighted images and high signal intensity on T2 weight images. Blastic mets appear with low signal intensity on both T1 and T2 weighted images. Bone scans are sensitive but not specific, and can be used to screen the entire skeleton for sites of metastatic disease. Clinical Significance: Patients with metastatic cancer are usually older (>40 YOA) and 10- 15 years after the primary was diagnoses. They will present with insidious onset of pain and/or pathological fractures. The pain will often also present at night (DDx for night pain is bursitis). They will have unexplained weight loss and cachexia (overwhelming state of being unwell, fatigue, pallor, malaise, drastic weight loss regardless of nutrition, pale, sunken cheeks, drawn face, gaunt), and in late stages anemia and fever. As a

Bone Metastasis
Metastatic bone tumors make up 70% of all malignant bone tumors, while only 30% are primary. The most common primary malignancies are lung, breast, prostate, kidney, thyroid and bowel. 80% of the time, the primary is from breast, lung, prostate or kidney. In kids less than 20 YOA, 80% of the time the tumor is from a neuroblastoma, and 50% of the time is due to Hodgkins Lymphoma. Cancer cells from primary lesions spread to other parts of the body in three ways. The most common route of spread is by hematogenous routes (metastasis through the blood stream, either arterial or venous, the venous plexus is the largest source of mets to the spine because this is an area os slow blood flow). The cancer cells spread to the red marrow in bones of the axial skeleton (Batsons Venous Plexus). The second route of spread is lymphogenous (metastasis through lymph channels and deposits in lymph nodes), and the third route of spread is by direct extension (direct invasion into bone from adjacent soft tissue tumor) for example, from the uterus to the pelvis). Metastasis can be lytic, blastic or mixed. Lytic are most common (75%) and can be separated into two different presentations. Lytic lesions can appear as blown out metastasis, which accounts for 10% of all metastatic lesions. Blown out mets are usually solitary lesions, with primaries in the thyroid, kidney and lung. They are usually in the axial skeleton and usually are not found in the vertebral bodies. A differential diagnosis for blown-out metastasis is the solitary plasmacytoma. The most common primary tumors to cause lytic mets are from the lung, breast, kidney and thyroid, however, all primary tumors except for CNS tumors and basal cell carcinoma can metastasize to bone. Prostate cancer likes to metastasize to bone, however it produces a blastic metastatic lesion. Mixed metastasis is a combination of lytic and blastic metastasis, and there must be cortical destruction in order to call a lesion as mixed. Multiple myeloma cannot be considered as a differential diagnosis for mixed metastasis because multiple myeloma does not have sclerotic metastatic lesions. However, multiple myeloma can be a differential for lytic mets. You can distinguish the

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general rule, with a primary cancer metastasizes to bone, the prognosis is not good. There is generally not soft tissue swelling with metastatic disease. Differential diagnosis for a lytic, bubbly ilium include: lytic (blown out) metastasis if the patient has pain and is over 40 YOA, multiple myeloma or plasmacytoma if the patient has pain and is over 50 YOA, fibrous dysplasia if the lesion is painless and regardless of age, a brown tumor from hyperparathyroidism which may or may not produce pain, or a hemophiliac pseudotumour which may or may not produce pain. Differential diagnosis for an ivory vertebrae includes blastic mets, pagets disease (which should also show expansion) and Hodgkins Lymphoma. Laboratory Findings of Metastatic Bone Disease: In lytic metastasis, serum calcium will be high. In blastic metastasis, alkaline phosphatase will be high. In prostate cancer, acid phosphatase will increase. ESR (erythrocyte sedimentation rate) will be high (ESR can increase from almost anything). Management: These patients need to be referred. If the mets are in the spinal column, collar & holler, then do a neurovascular exam. Drop Metastasis This occurs when neoplastic cells spread throughout the CSF (cerebrospinal fluid). They drop according to gravity and motion. Most commonly, drop mets will ssed in the lumbar spine because of gravity. Radiographic findings: Drop Metastasis are not seen on x-ray. MRI will see nodular thickening of the meninges. Clinical significance: Symptoms are very subtle. Lytic Metastasis Tumor cells deposit in the bone marrow because of Batsons Venous Plexus. Pressure from proliferating neoplasms on the surrounding bone causes reabsorption of the trabeculae. Radiographic findings: These are lytic lesions. The winking owl sign might be seen. Blastic Metastasis Blastic metastasis have increased bone density from the laying down of new bone. Mixed Metastasis In mixed metastasis, there are many foci of both blastic and lytic metastasis.

39 Blown-Out Metastasis Blown-out metastasis is a type of lytic metastatic focus that creates a soap bubbly lytic appearance. Blown out metastasis is common in renal or thyroid cancers. Radiographic findings: These lesions are lytic, and soap-bubbly. Blown out metastasis are exceptional in two ways, because unlike most metastatic lesions, they do create a soft tissue mass and they can have periosteal reaction.

BONE INFECTIONS
Osteomyelitis Infection of Bone
There are two major forms of osteomyelitis: pyogenic (pus-forming) and non-pyogenic (non-pus forming, granulomatus, Tuberculosis is the most common). Pyogenic infections involve a microorganism (Staph Aureus most commonly) spreading the infection hematogenously from the site of the primary infection (UTI, URI, skin, teeth) to the bone. There are four categories of pyogenic infections: acute, sub-acute, chronic, or Brodies Abscess. Non-pyogenic infections usually start in the lungs, and then travel to the bone via the blood (or the GI). There are four pathways of extension of an infection: hematogenous spread (which is most common), contiguous source, direct implantation, or post-operative. Tissues involved in infections are the soft tissues (cellulitis), articulation (septic arthritis at or including the joint), cortical bone (osteitis), or medullary bone (osteomyelitis, within the shaft of the bone). Septic means that the infection was caused by some bacterial organism. *Infection usually only affects one level, whereas TB can affect more than one level. *DDx for unilateral sacroiliitis: Infection (until proven otherwise), RA, Psoriatic arthritis, Reiters Syndrome (reactive arthritis). *Drug abusers are prone to infection of the S- Joints: Spine, Sacroiliac, Sternoclavicular, Sacroiliac, Sternoclavicular, Symphysis Pubis (also more prone to gram negative organisms). Infectious spondylitis involves a focal deviation of the paraspinal line at the affected level, disc and adjacent vertebral body destruction, prevertebral abscess, and a kyphotic angulation. Discitis involves disc space narrowing and destruction of the adjacent vertebral endplates. Vascular anatomy: infants under one year of age have metaphyseal vessels which penetrate the growth plate, and infections love to set up in the metaphysis. Because of this, there is a very high risk of spread to the epiphysis and to the joint in infants! Between the years of 1 and skeletal maturity, the metaphyseal vessels cross the physis.

 Infections will spread hematogenously to the metaphysis, and spare the epiphysis and joint. When the patient is an adult, the physis is no longer present, so there is an increased risk of septic arthritis spreading to the joints. So if the patient is under one years of age or is an adult, the infection will result in septic arthritis because the infection is able to spread to the joint. From the age of one to adulthood, the infection will stay in the metaphysis and result in osteomyelitis.

40 The laboratory findings associated with infections include elevated ESR, WBC may or may not be elevated (however WBC is more commonly elevated with extremity infections), positive blood in joint cultures, and sputum may be positive in tuberculosis.

Clinical significance: Patients will generally be in their 50s or 60s, and a high association with bone infections and UTIs. Signs and symptoms depend on the organism and the patients resistance. Infections start in the metaphysis, but if left Some important terminology to know: untreated, the infection may spread to the epiphysis and joint, depending on the persons age. Patients with pyogenic infections will present with a fever (infrequently in - Sequestrum: segment of necrotic bone that looks white, and lacks blood supply. adults, and in 1/3 of children), severe and constant pain, malaise, anorexia and the chills, - Involucrum: a collar of living bone surrounding the sequestered bone. Living swelling/heat in the superficial area, and decreased range of motion if the infection bone around the infection responding to the infection. involves a joint. *TB takes months and months to grow. Pyogenic infections grow must - Cloaca: Is a defect in the involucrum which allows drainage of the inflammatory faster. History is important. products. A cloaca is a channel to drain the pus (to the surface of other organ Management: If the patient has an acute infection, sent them to the ER now! structures). - Marjolins Ulcer: is a rare complication of infection in which a squamous cell Suppurative Osteomyelitis carcinoma develops in the location of a previous cloaca. There is an increased frequency of suppurative osteomyelitis in the Radiographic findings: The radiographic latent period before you can see an infection is immunocompromised patients, alcoholics, newborns, and drug addicts. It is most 7-10 days if the infection is in the extremities (learning tool: you have ten fingers and ten commonly between the ages of 2-12 years of age, and affects males to females 3:1. S. toes in your extremities), and 21 days if the infection is in the spine. The first thing you aureus is responsible for 90% of all bone and joint infections. will see is soft tissue swelling with a blurred/obliterated muscle/fat interface which can be present within 3 days of the bone infection. A moth-eaten or permeative type of Acute Pyogenic Osteomyelitis bone destruction may be seen that usually originates in the metaphysis of tubular bone Radiographic findings: The first sign is soft tissue swelling and a blurred muscle/fat first. Periosteal reactions (single layer, laminated, Codmans Triangle) and cortical bone interface. Moth eaten or permeative bone destruction, usually in the metaphysis. destruction will be present. There will be continued elevation of the periosteum and Periosteal reaction is single layered, laminated or solid. Acute pyogenic osteomyelitis new bone formation which can result in a large involucrum. If the infection is near a spreads very rapidly. joint there will be rapid destruction of the joint with cortical destruction on both sides. This will help differentiate between tumors (which do not like to cross joints) and Subacute Pyogenic Osteomyelitis infections. May see paraspinal or prevertebral abscess. Disc space narrowing with The major difference between acute and subacute pyogenic osteomyelitis is time and irregular vertebral endplate destruction. Intradiscal gas is extremely uncommon in spinal the patients history. infection. *To differentiate tumor from infection, know that tumors usually do not cross or affect joints, whereas with infections, the joint can be involved! Radiographic findings: There will be a moth eaten pattern of bone destruction, periosteal reaction, pre-patellar soft tissue swelling with obliteration of ST planes. . 90% of the time, the infection is located in the appendicular skeleton, while only 10% of the time the infection is in the spine. Chronic Pyogenic Osteomyelitis On MRI, there will be a low signal intensity on T1 weighted images and high signal intensity on T2 weighted images and fat suppression images (including involved discs) There will be destruction of cortical bone (on both sides of a joint) and soft tissue destruction. Chronic pyogenic osteomyelitis will occur if the acute form is not treated properly in the acute phase, and is a continuation of the acute form. Bone destruction and joint destruction increases, sclerosis increases, and pieces of the bone dies (sequestra, areas of dense bone surrounded by lucency). The periosteal reaction continues, thickens and attempts to wall off the infection (involucrum). The end result is a thickened bone with sclerotic vortex and a wavy outer margin. *The chronic form will look much worse than the acute form because the body is trying to wall off the infection, but the real difference between the acute, subacute and chronic forms is time.

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Radiographic findings: Increased density of the involved bone, most commonly in the tibia. There will be sclerosis, cortical thickening, bone destruction, periosteal reaction (involucrum), pieces of bone that will separate and die (sequestrum). Management: These patients need referral for surgical debridement and stabilization. break in the cortex of the metaphysis. Normally the open growth plates inhibit the spread of infection from metaphysis to the epiphysis and the joint.

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Radiographic findings: Tom Smiths Arthritis loves the proximal and distal femur, distal tibia, proximal and distal humerus.

Brodies Abscess

This is aborted osteomyelitis (OM) and a localized form of suppurative OM. Brodies Abscess generally appears as a low grade infection in kids. Often there are no microorganisms when cultured. Differential diagnosis for a Brodies Abscess is an Osteoid Osteoma, or osteomyelitis. They may even have the same history. The pain is also relieved by aspirin. Radiographic findings: Very similar to an osteoid osteoma with a radiolucent nidus/abscess, however the nidus of the brodies abscess is larger than the osteoid osteoma (closer to 2 cm). There is also a halo rim of sclerosis that is usually thicker and more irregular. Bone scans will be hot because there is lots of blood going to the bone. Clinical significance: The signs and symptoms resemble an osteoid osteoma. The pain is worse at night and alleviated by aspirin. Management: Refer these patients to their GP quickly, then to a surgeon to have the nidus removed.

Non-Suppurative/Non-Pyogenic Osteomyelitis, Tuberculosis TB

A third of the worlds population has latent tuberculosis, with 9 million new active cases annually. Most cases are seen in India, China, sub-Saharan Africa, Indonesia, the Philippines, Afghanistan, Bolivia and Peru. Rates are increasing in North America and Western Europe in the past 15 years because of immigration, HIV/AIDS and neglect of TB control programs. There are several predisposing factors to TB: HIV, AIDS, ETOH abuse, intra-articular steroids, prolonged systemic illness, malnutrition, poor hygiene, and overcrowding. If TB appears in the spine, it is called Potts Disease and can affect more than one adjacent segment of the spine, however, patients usually will not get multiple infections. Remember the tube story from England. In crowded places, TB spreads fast. TB usually occurs in places with low socio-economic status, poor and highly populated and low-hygienic places. Radiographic findings: Early signs include lytic endplate destruction, loss of disc height, anterior gouge defects, paraspinal swelling (retropharyngeal, retrotracheal, paraspinal line, and psoas). Advanced signs include vertebral body collapse, gibbus deformity and obliteration of the disc. TB likes the hips and knees. Usually you cannot TB from differentiate from pyogenic infection, you need a history in order to differentiate the two. There may be a gibbus deformity (excessive/acute/abrupt thoracolumbar kyphosis from bone destruction), and may have cold abscesses with snow-flake calcifications, especially in the psoas muscles. Phemisters Triad for TB of a peripheral joint involves progressive and slow joint space narrowing, juxtaarticular osteoporosis and peripheral erosions of the articular surfaces. If the lesion is not very sclerotic and has a periosteal reaction, think of a chronic lesion. Clinical significance: If TB appears in the spine (Potts Disease, then paraplegia may result. Lab results are often normal (+PPD). TB is becoming resistant to drugs (especially in eastern Europe, China and Iran). Infections can eventually burn themselves out. Management: Chemotherapy is usually quite effective, and has recently been shown that causative organism is becoming quite resistant to modern drug therapy. Surgery is seldom.

Septic Arthritis

Septic Arthritis is most commonly from blood borne pathogens, from a distant focus of infection and direct implantation, most commonly S. Aureus. Radiographic findings: Usually monoarticular involvement at the hip or knee. Earliest sign is distention of the joint capsule. Waldenstroms Sign (indicates joint effusion). Increased teardrop distance (>11 mm or >2 mm difference from contralateral side). Joint destruction rapidly follows. Clinical significance: The earliest signs are inflammation and swelling. 4 weeks later, the patient will have rapid narrowing of the joint space and bone destruction (femur, ilium, ischium most commonly). Three months later, there is bone destruction with dislocation of the hip, AVN of the femoral head, sequestrum in the ischium and femoral head (sclerosis). You will also see pain, erythema, fever, elevated ESR and leukocysosis.

Tom Smiths Arthritis

Bones that have their metaphysis within the joint capsule are predisposed to rapid development of septic arthritis. Infection then can spread to the synovial fluid from a

TB Spondylitis (Potts Disease)

Disc and VB destruction resulting in Gibbus deformity. Psoas abscess. Paraspinal soft tissue stripe. (In all infections).

Tubercular Arthritis

Tubercular Arthritis has a longer period of onset than the pyogenic form. Radiographic findings: Tubercular arthritis loves the spine, hip and knee, and appears very similar to pyogenic osteomyelitis, except there is less sclerosis. There may be a cold abscess. Clinical significance: Slow and insidious onset.

42 cocciciodomycosis can mimic tuberculosis with multi system infections. Most of these infections are indolent, low grade and self-limiting. Actinomycosis Is a bacterial infection usually found in the mouth and bowel, which usually doesnt cause problems unless they get lodged in devitalized tissue or introduced into deep tissues from an open wound. Bone infection is usually caused by direct extension of adjacent ST infections. Maduromycosis Most commonly fungal skeletal infection worldwide. It affects primarily the feet (Madura Foot), and is most common in tropical regions, with the highest incidence in India. The skeletal infection is from adjacent soft tissue infection.

Syphilitic Osteomyelitis

Syphilitic osteomyelitis is rare since penicillin was invented. The basic lesion is an angiitis of the small arterioles that leads to necrosis of the vessel wall and infarction of the tissue supplied by the vessel. The end result is a gumma that consists of areas of coagulative necrosis surrounded by infiltrate of plasma cells and leukocytes.

PAGETS DISEASE (THE GREAT MIMIC)

Pagets Disease was named after Sir James Paget in 1877, and is also known as Osteitis Deformans. It is defined as an increased osteoclastic activity, with osteoblastic response causing disordered bone formation and highly vascularized tissues that often puts stress on the heart. 3% of people over the age of 40 in certain geographic regions have Pagets, and it is most common in the UK, Australia, and New Zealand. It likes elderly Caucasian patients, males more than females. Its etiology is likely viral (from paramyxovirus or a family of measles virus), but is really not known. Pagets could also result from chronic inflammation, or viral infection. It is usually polyostotic (85%), but can be monostotic as well (15%). Monostotic versions usually involve the tibia, skull, pelvis, spine and femur. It loves the axial skeleton and proximal femur. There are four stages of Pagets disease. The first is the lytic, destructive and monophasic phase, and the lesion will look like a well-marginated lucent lesion at this stage (characterized by OP circumscripta, blade of grass sign in tibia, osteopenic bones, bone expansion, pathological fracture, coarse trabecular bone, ground-glass sign). The second phase is the mixed phase. The mixed /combined/biphasic phase is most commonly seen and involves lytic areas with thick cortices, coarse trabeculae, bony expansion and signs of bony softening (characterized by Cotton wool skull, patchy looking bone, increased radiographic density in the bones, and a picture frame vertebrae). The third phase is the sclerotic phase, which is when the bony is purely opaque, expanded and signs of bone softening are evident (you will see thick and coarse trabeculae). You may see bone bowing in this stage. The fourth stage is malignant degeneration involving cortical destruction, soft tissue mass, and possible periosteal reaction, however malignancy from Pagets is rare. If it does present, usually the changes are lytic in nature, and the bone scan may be cold, except with a sarcoma in which case the bone scan will be hot. *One possible differential diagnosis when in the spine is hemangioma, however hemangioma do not have thickened cortices. In order to diagnose Pagets you must see bone expansion. Check from right to left to compare if possible. Differential diagnoses for Pagets include: vertebral sclerosis (hemangioma,

Congenital Syphilis

Congenital syphilis is transmitted through the placenta from the mother to the baby. There are three phases. The first is metaphysitis, and there will be bilateral and symmetrical radiolucent metaphyseal bands with a saw toothed appearance. Symmetrical erosive defects on the medial surface of the proximal tibia represents Wimbergers Sign of syphilis. The second stage is periostitis, which appears bilaterally and symmetrical, solid or laminated. The third stage is osteoitis, which is when there is spread to the diaphysis. This often results in anterior blowing of the tibia known as a saber shin. Clinical Significance: If congenital syphilis if untreated, 25% die in utero and 25-30% will die shortly after birth. The patient may present with Cluttons Joints, which is when there is bilateral and painless joint swelling, but there may be warm and painful. Hutchinsons teeth may also be present, when the patient has deformities of the teeth in which they look notched, and peg-shaped.

Acquired Syphillis

Skeletal changes are seen in tertiary syphilis, and are only found in 10% of patients. Radiographic findings: Superficial bones (ex: skull, tibia, clavicles) are most commonly involved. The most common sign is proliferative periostitis.

Mycotic Osteomyelitis

Most fungal infections are secondary to a primary respiratory infection or from direct extension from an adjacent ST infection. Coccidiodomycosis This is an endemic in southwestern US, where the skeletal infection is usually secondary to pulmonary infection. The signs and symptoms of

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metastasis, and lymphoma). IN these cases, bony expansion is key. Blastic mets may occur in the pelvis, but these lesions are usually cortically placed. If in the skull, the lesion may be fibrous dysplasia, hyperostosis, frontalis interna or metastatic disease. Distribution of Pagets: The pelvis is affected in 30-70% of patients with Pagets. In these patient there will be a loss of the Kohlers teardrop distance, trabecular and cortical thickening (pelvic brim sign) and protrusio acetabuli). The sacrum is affected in 30-60%. The spine is affected in 30-70%, especially in the lumbar spine. There may be an ivory vertebrae, fish-shaped vertebrae, or neurological compromise. Pagets may target the skull in 25065% of patients wit Pagets. If in the skull, there will be osteoporosis circumscripta (cotton wool), bone enlargement, compression of the cranial nerves, CSF flow may be altered and compression of the brain tissue is possible. The facial bones are rarely affected. Basilar invagination is also possible. Pagets likes the long bones (25- 30%), and there may be bowing deformities, pseudo fractures (saber shin deformity, blade of grass deformity), pathological fractures, sheppards crook deformity (also seen in fibrous dysplasia), or malignant degeneration. Pagets is monostotic in 35% of cases, and polystotic in 65%. Radiographic findings: Pagets can be monostotic or polystotic, loves the axial skeleton and is characterized by bone expansion in the affected region, with very stringy trabeculae. If Pagets affects the pelvic rim, a brim sign might be seen where the cortices along the pelvic rim become thickened. If the spine is affected, you may see a picture frame vertebra, with decreased vertebral body height centrally, and the vertebra will appear wider than adjacent segments, with a sclerotic borders making it look like a picture frame. Bowed bones are common in Pagets from the bone softening. See the above stages for more detail. *If you see increased bone density in the pubic bone, this can be an optical illusion. You must see expanded cortices and thickened bone. Pagets will be hot on a bone scan. Clinical significance: Most often Pagets is asymptomatic (80-90%), and is found randomly in radiographic findings for another reason. Pagets can occur in multiple bones and can be found anywhere, even in sesamoid bones. There may be associated neurological compromise if the spine is involved (because of bone expansion), and spinal stenosis can be a problem. There may or may not be dull pain (especially if malignant degeneration has occurred), and if the bone expansion is superficial, this may be noticed clinically. The patient may complain of an enlarged hat size (because his/her skull is getting thicker and heavier) which can result in basilar invagination because the head is getting heavier, and softer, and sinks into the cervical spine. The patient may have muscle weakness, paralysis and incontenince. The cranial nerves can be affected (ex: deafness) from the bony changes and expansion. May get malignant degeneration (1- 5%), or early degeneration of joints. If malignant degeneration occurs, 50-60% of the time the resulting lesion is an osteosarcoma, and 20-25% of the time it is a fibrosarcoma. Chondrosarcomas are also possible. The patient may be anemic (because there is a ton

43 of blood pouting into the Pagetoid bone), and the patient may have a high output cardiac failure. There is often heart problems associated with Pagets from increased heart rate and cardiac output, or calcification of the vasculature or cardiac valves. The patient may suffer from fractures as well. Laboratory findings include: Increased alkaline phosphatase, increased urinary hydroxyprolene (indicates bone destruction because it is secreted from bone), hypercalcemia and hyperphosphatemia if the patient has a fracture. Management: Because the bones are soft, when adjusting these patients you must be VERY gentle and not body drop. These patients bones may break easily! Supportive braces may be necessary if to prevent extensive bone deformity. These patients should be referred to a medical doctor for prescription of medications to prevent further bone loss. Pharmaceutically, diphosphonates are used, mithramycinates help to stop the pathological changes. You cannot reverse the changes that have already occurred, you can just stop progression.

HEMATOLOGIC DISORDERS
Sickle Cell Anemia
SCA is an abnormality in Hb that causes the RBC to form a sickle shape. It is a chronic, congenital and hereditary hemolytic anemia. Is it almost exclusive to black individuals as well as certain Mediterranean populations. SCA is protective against malaria. SCA results from an abnormal structure of hemoglobin, which sickles under low oxygen tension, causing hemolysis and vascular occlusion and tension hypoxia (blood flow to the centre of the endplates stops while the periphery will continue to grow). Radiographic Findings: H-shaped Vertebrae (due to vascular compromise to the middle of the endplates from sickling, they look like schmorls nodes on multiple levels making the vertebral body look like the letter H). Infarctions/AVN (patchy sclerosis), small/absent spleen, patchy bone sclerosis. AVN + Dense Bones = SCA. Clinical Significance: SCA may not be symptomatic, or may have abdominal crises, jaundice, bone pain and dactylitis. Patients will be predisposed to salmonella osteomyelitis. The patient may also have infection, visceral infarcts, and cardiac decompensation. Patient will present with pallor, weakness, episodic abnormal crisis due to vaso-occlusion and ischemia, jaundice and acute low back pain.

Thalassemia
This is also called Cooleys Anemia or Mediterranean Anemia. It is a disorder of hemoglobin synthesis (poor RBC formation) and comes in three forms, major, minor and

 intermediate. The major form is homozygous, the minor form is heterozygous. This is the most severe of all anemias. Radiographic findings: Hyperplastic marrow and widening of the medullary cavities with thinned cortices, expansion of bone, and thickened trabeculae. Hair on end alpha marrow proliferation (marrow space enlarges and can have extrusion from tables) Clinical significance: The patient will often have a large liver and spleen, causing extramedullary hemoatopoiesis paraspinal soft tissues masses. The patient will have pallor, lethargy, and retarded growth. Hepatosplenomegaly and maxillary over-growth (rodent faces) are common. Laboratory abnormalities include: Hypochromic Microcytic anemia Reticulocysosis Nucleated RBCs Target cells (abnormal RBCs) Elevated bilirubin

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Hemophilia
This is an x-linked recessive condition involving coagulopathy (deficiency in a specific blood clotting factor). It only occurs in males. It is most characterized by a deficiency of clotting factors VIII or IX. It is uncommon, and looks nearly identical to JRA (with a squared patella and wide intercondylar notch). The two most common bleeding disorders with skeletal abnormalities are Hemophilia A and B. Hemophilia A is also known as Classic Hemophilia and Hemophilia B is also known as Christmas Disease. Both are sex-linked recessive and females are carriers, and the disease usually manifests in males. Radiographic findings: Skeletal changes from hemorrhages within/around joints. Intraosseous hemorrhages look expansile, lytic and often called a pseudotumor (bleeding into a bone, making a small to large pocket of blood in a bone). MC in the weight bearing bones such as the ilium and femur. Bones generally osteopenic. Osteoporosis and overgrowth of epiphyseal region from increased blood flow. Inability to see articular margins. Widening of the intercondylar region, with many cysts in subchondral regions. Periarticular osteoporosis, subchondral cysts, dense soft tissue swelling (from hematomas), decreased joint space. Not an x-ray diagnosis. Clinical Significance: intra-articular hemorrhages can cause permanent changes, and hemophilic arthropathy. Dense effusion from bleeding within the joints. Anytime you have blood in a bone (excessively) it will appear more osteopenic. Usually presents at about 6 months of age. No trauma is necessary for the hemorrhages, often they are spontaneous.

Sickle Cell Dacylitis

This is an inflammation of the digits associated with SCA. It is common in infancy, and is also known as hand and foot syndrome, because its found in the small bones of the hands and feet. Radiographic findings: Coarsened trabeculae, wider medullary cavities, reactive hematopoesis causes cortical bone to be thinned, and the diaphysis will not be remodeled how it should and then appears wider. Clinical Significance: The patient will present with painful swelling of the hands and feet from early infarction or infection. Cold weather aggravates the condition.

Leukemia
Leukemia is more specifically known as Acute Lymphocytic Leukemia (ALL). It is the most common malignant disease in kids 2-5 YOA. This is a malignant disease of marrow from proliferating white blood cells. Can occur in childhood (acute) or adulthood (chronic). Acute leukemia is the most common childhood malignancy. Osseous changes are most commonly found in kids. Usually fatal in one year. *Any childhood disease can cause radiolucent sub-metaphyseal bands. Radiographic findings: Radiographic findings are only seen in 50-70% of kids with leukemia. Osteopenia, radiolucent submetaphyseal bands (white lines running horizontally near endplates smaller trabeculae in this area). Bone destruction, perioritis (periosteal reactions tend to be bilateral, and usually single solid or laminated). Lytic lesions and periosteal reactions. Management: To make a definitive diagnosis, take a bone marrow biopsy, and blood tests. This is a clinical diagnosis. The patient will present with generalized bone pain, weakness, lethargy, lymphadenopathy (swollen lymph nodes), splenomegaly, pallor and generalized malaise.

AVN of the Femoral Head

AVN of the femoral head is associated with SCA as well. Ischemic changes in SCA patients occur in 8-20% of patients. There is an avascular stage, which leads to a revascular stage, which leads to deformity. The infracted area appears bright white. Overall may see a patchy appearance, identical to idiopathic and post-traumatic forms. Radiographic findings: Sagging rope sign, increased teardrop distance (from joint swelling), Snow cap sign (in revascularization phase), subchondral cysts, Bite Sign, Crescent Sign (indicates subchondral fracture).

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45 subcortical fracture (crescent sign), and cortex collapses (step defect). Deformity and fragmentation will occur. The third phase is the repair and remodeling phase which can last 1-2 years. Bone is deposited and some deformity occurs, and the epiphysis reconstitute. There is a gradual return of normal bone density. The last phase is the deformity phase, and follows healing. Residual deformity of the articular surface results. Radiographic findings: Sclerosis, fragmentation, collapse, crescent sign (crescent-lucency on weight bearing surface), lytic lesions, and joint surfaces should be normal. Subchondral cysts are often evident in the region of the greater articular stress/weight bearing joints. The best imaging modality for AVN is MRI (its both sensitive and specific).

Osteonecrosis
Osteonecrosis is the death of bone cells and marrow from vascular compromise. The etiology can be spontaneous (most commonly for epiphyseal), trauma, alcoholism (fatty emboli occurring), corticosteroid use (asthma, rheumatoid arthritis, patients with kidney transplants), Caisson Disease (Deep Sea Divers), Gauchers hemoglobinopathy, collagen vascular (RA, SLE), Radiation, pancreatitis, and gout. Osteonecrosis is commonly located in metadiaphyseal region (DDx: enchondroma) or epiphyseal regions (where it could affect the joint). In the epiphysis: osteonecrosis can cause collapse of the articular surface leading to pain and altered joint function. Early diagnosis and treatment is important to minimize disability. There are four phases of osteonecrosis. The first stage is the avascular stage where there is cell death occurring within 2-4 hours. You will only see this on bone scan. The second stage is the revascularization stage, where new vessels infiltrates around the periphery and new bone is deposited onto the dead bone leading to increased bone density. Dead bone is resorbed. The third stage is the repair and remodeling stage. Bone is deposited, new bone is plastic, and will deform with weight bearing. The fourth stage is the deformity stage, the end product, the less deformity the better. Clinical Significance: this is a self-limiting condition lasting 2-8 years. The patient will not be weight bearing in the revascularization phase of the repair/remodeling phase because the dead bone is brittle and the bones are very weak. Radiographic findings: if you see subchondral fractures, there isnt anything you can really do beyond this point. The radiographic findings are pretty well the same as the avascular bone conditions as above. Clinical Significance: Osteonecrosis can be asymptomatic or painful. Signs and symptoms can vary.

Metaphyseal/Diaphyseal AVN
Decreased blood flow to the metaphyseal/diaphyseal region of bone. Radiographic findings: Usually occurs in the medulla (central) but can involve the cortex. Loves the weight bearing bones such as distal femur, proximal tibia or proximal humerus. Mature infarcts develop as well defined, undulating/serpinginous rims of sclerosis. Cortical infarcts are most common in small tubular bones of the hands and feet. If you ever have increased blood flow to a region to will seem osteopenic. If you have decreased blood flow to an area, it will seem osteosclerotic. Clinical Significance: rare complications such as transformation to malignant fibrous histiocytoma (MFH) of fibrosarcoma.

Medullary Infarction
Decreased blood flow to the medullar region of bone. Radiographic findings: central lesion with a serpiginous rim of sclerosis. May get more sclerotic as it matures. On MRI, there will be a high signal zone surrounded by a serpentine, thin, low signal border. Use T1 weight images to assess bone marrow! If this condition is suspected, do a bone scan first. Clinical significance: If the patient has had a previous necrotic event in the past, it can recur to make sure to rule this condition out. A rare complication is malignant degeneration to fibrosarcoma.

AVN (Hip and Spine)

AVN Stands for avascular necrosis, and can be caused by acute trauma, corticosteroids and alcohol abuse most commonly. Less commonly, AVN can be caused by Caissons disease (deep sea divers), Cushings disease (when the body produces too many corticosteroids), Sickle Cell Anemia, Gauchers, chronic pancreatitis, radiation therapy, or it can be idiopathic. There are four phases of AVN: avascular, revascular, repair/remodeling and deformity. The avascular phase lasts for 0-12 months and have no radiographic findings. There may be increased joint space from swelling and disuse osteoporosis. The second stage is revascularization which can last from 6 months to 4 years. Bone is deposited and resorbed, resulting in sclerosis, in particular the snow cap sign. There may be a

Legg-Calve-Perthes Disease
AVN of the femoral head before closure of physis (which is usually between the ages of 3-12, peaking around 5-7). It is self-limiting with 2-8 years, resulting in greater deformity at older ages of onset. 5:1 male to female ratio. 10-20% are bilateral. Rare in black individuals. Familial in 6-12% of cases.

 Radiographic findings: small capital femoral epiphysis (early on), sclerosis of the femoral head, widened joint space (joint fluid ligamentous laxity), destruction of the articular cortex, crescent sign (subcortical lucency from subchondral fracture later on in the disease), fragmentation of femoral head, epiphysis of femoral head will look crumbly, fragmented and patchy. Mushroom cap deformity (femoral head looks like a mushroom), sagging rope sign (articular cartilage all around the large, mushroom-like femoral head), residual deformity after healing. Crumbly-looking epiphysis, which are fragmented and patchy. Bone scan: low-signal intensity (femoral epiphysis) on T1, intra-articular effusion, femoral head deformity, photophenic area in the proximal femoral epiphysis (from blood supply being cut off to the epiphysis). CT: collapse of the head, curvilinear sclerotic zone, areas of lowered attenuation in the head and intraosseous cysts. Clinical significance: self-limiting, resolves in 2-8 years with various degrees of deformity. Management: Divide the femoral head into 1/3s: medial, middle and lateral pillars. The femoral head will collapse medial to lateral. When the lateral side of the femoral head collapses/crumbles, then the patient needs surgery. Must refer the patient to an orthopod early on (even if just for x-ray or MRI). The patient should be re-x-rayed in 6 months. Patient may need hip replacement later in life. >50% do not require treatment. Instruct patient to have minimal weight bearing, initiailly. Bracing or surgery can help maintain abduction and hip rotation. With revascularization, there will be reformation of the femoral head.

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Freibergs Disease
This is AVN of the metatarsal head, most commonly with the second metatarsal. 13-18 years of age, and there is a 5:1 female to male ratio. This can be secondary to trauma or increased stress. Radiographic findings: the involved head appears enlarged, flattened and fragmented.

Keinbocks Disease
AVN of the lunate. 20-40 year olds. 9:1 Male to female ratio. There is bone resorption, deposition, fragmentation and collapse. Associated with negative ulnar variance, the ulna is shorter than the radius. Radiographic findings: negative ulnar variance in up to 75% of the cases. Radiographs are negative for months, then the lunate will appear increased in density. Later on there will be fragmentation and collapse with mixed density.

Spontaneous Osteonecrosis of the Knee (SONK)

SONK usually occurs in people over 60 years of age, and it is of unknown etiology. Most commonly in the medial femoral condyle in adults. Radiographic findings: initially the films are usually negative. The earliest finding is flattening of the articular surface. May see detached osteochondral fragments which can become loose bodies or joint mice. Subchondral bone density is mixed sclerosis and lucency. The crescent sign indicates a subchondral fracture. MRI and Bone Scan positive early. Long latent period for plain film radiographs. This has the same appearance as other disorders (steroid induced AVN, hemoglobinopathies, and transplantation). Clinical Significance: if the defect occupies >50% of the articular surface, surgical arthroplasty is indicated.

Spontaneous Osteonecrosis of the Femoral Head

This is AVN of unknown causes, also known as Chandlers Disease. There is a 4:1 male to female ratio and is bilateral in 50% of cases. Radiographic findings: radiographically similar to other disorders with osteonecrosis of the femoral head. Will go through the same phases!

Osgood-Schlatters Disease
This is not AVN, but patellar tendinitis, or partial disruption of ligament attachment (patellar ligament at tibial tuberosity). 11-15 year olds most commonly. More frequent in males. Bilateral 25-50% of the time. Radiographic findings: considered a clinical diagnosis. Clinical significance: the patient will present with pain at the patellar tendon/tibial tuberosity complex. Pain on resisted extension.

Caisson Disease
Decompression sickness, AKA The Bends. Most common in scuba divers who ascend from a depth too quickly. Radiographic findings: Results in epiphyseal metaphyseal and diaphyseal osteonecrosis. Appears identical to the spontaneous form. Clinical significance: Nitrogen bubbles come out of the solution in your blood and act as emboli and result in osteonecrosis.

Osteochondritis Dessicans (OCD)

OCD is most common in the knee on the lateral aspect of the medial femoral condyle. The second most common location is the ankle on the medial aspect of the talar dome.

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The third most common location is the capitellum (Capitulum), which is common in little league pitchers. OCD is common in active patients between 20- and 30 years of age. There is an unknown etiology in children and adolescents. Most common in 11-20 year old males in knee, ankle, elbow and hip. There may be a history of acute trauma. The separated fragments can get reattached, displaced into the synovium. The fragment can get embedded or move freely, or may get resorbed. It likes to target the femoral condyles, talus (medial talar dome following an ankle sprain, hip, patella, foot (metatarsal heads), shoulder, elbow (capitellum/capitulum), wrist and TMJ. Radiographic findings: Small necrotic segments of subchondral bone. The fragment may become a loose body. May not see joint mouse because it may be cartilaginous (cant see on x-ray) or it could be so small that we cant see it. On MRI necrotic area appears low signal on T1. Clinical significance: Swelling, pain, clicking or locking.

47

Severs Disease
Thought to represent AVN of calcaneal apophysis.

Singing-Larden-Johansson Disease
Similar to Osgood-Schlatters, only when the patella is affected.

Arterial Disorders
Atherosclerosis
This is the most common degenerative disease of the human race. Its incidence increases with age, diet and family history. It is a plaque build up in the arterial vessels. Radiographic findings: to see atherosclerosis on x-rays, the plaques must have calcified (conduit wall calcification). Most common in the abdominal aorta (L3-4). The aorta should be within 5 mm of the spine, if larger could indicate a soft tissue mass. Aorta should measure less than 3.8 cm otherwise an aneurismal dilation is present.

Blounts Disease
Growth disturbance at the medial, proximal tibia.

Monchkebergs Medial Sclerosis

Monchkebergs Medial Sclerosis is when there is calcification in the media of small/medium muscular arteries. NOTE: Atherosclerosis occurs in the endothelial layer!. This condition is rare before 50 years of age. Monchkebergs Medial Sclerosis does NOT relate to the lumen of the vessel. Radiographic findings: Most commonly found in the femoral, tibial, radial, ulnar and genital arteries. You will see circular, ring-like densities along the entire length of the vessel. Clinical Significance: if you see Monchkebergs Medial Sclerosis, the first thing that should come to your mind is DIABETES.

Diazs Disease
AVN of the body of the talus after trauma.

Hasss Disease
AVN of the humeral head.

Kohlers Disease
AVN f tarsal navicular.

Mauclaires Disease
AVN of the metacarpal head.

Aneurysms
Aneurysms are an abnormal dilation of any artery or vein. It is most common in the aorta, splenic, renal and vertebral arteries. The most common peripheral location is in the popliteal artery. Cardiac aneurysms are most common in the left ventricle. Aneurysms can be congenital or acquired (most common as we age, and can include atherosclerosis, infection, poststenotic dilation, syphilis and arteritis). Radiographic findings: Curvy, linear, convex calcification. Clinical Significance: if you suspect an aneurysm, use advanced imaging. US is cheap and effective, CT and MRI also work but they take more time and are more expensive.

Panners Disease
AVN of capitellum in young males.

Preisers Disease
AVN of the scaphoid, not from a fracture.

 Radiographs will not show the aneurysm unless there is calcification or plaque. On physical exam, blood pressure will be elevated, and will be different side to side. Palpate over the are for pulsative mass, and auscultate (you may hear bruits). If someone has an abdominal aortic aneurysm, the anterior margins of the vertebral bodies will be bowed! This can present with musculoskeletal pain. To rule it out, sent the pt for an US.

48 Reflex Sympathetic Dystrophy Syndrome (AKA Complex Regional Pain Syndrome) This is a post-traumatic bone disorder causing acute osteoporosis. It occurs commonly in individuals over 50 years of age with a history of recent (trivial) trauma. Radiographic findings: Patchy, mottled osteoporosis, metaphyseal localization. Later, osteoporosis becomes more generalized. No joint disease. Clinical Significance: Patient will present with pain, swelling, atrophy distal to trauma site. Usually resolves in months-years. Disuse and Immobilization Osteoporosis The most common causes for disuse/immobilization osteoporosis is traumatic injuries with immobilization, motor paralysis, or inflammatory bone/joint lesions. Changes will being to appear on film after 7-10 days. Extreme changes will be seen by 2-3 months. This condition relates to the sympathetic nervous system having increased sensitivity due to trivial trauma. In the upper extremity, this type of osteoporosis can be very painful. Radiographic findings: There are four radiographic patterns of disuse atrophy: 1. Uniform, 2. Spotty bands, 3. Cortical lamination, and 4. Scalloping. Transient Regional Osteoporosis There is no associated cause of transient regional osteoporosis. It is sudden and reversible, affecting the peri-articular bone. Most common in 20-40 year olds in the hip. There are two entities: 1. Transient Osteoporosis of the hip and 2. Regional Migratory Osteoporosis. Regional Migratory Osteoporosis is mainly found in males, in the lower extremities. Localized regressing and migratory osteoporosis. Radiographic findings: Marked osteoporosis of the femoral head, which is less severe in the femoral neck and acetabulum. Clinical Significance: Can be associated with pregnancy, and in this case will most likely be found in the left hip. Transient regional osteoporosis reverses when the person starts stressing his/her bones. May be related to AVN.

Venous Insufficiency
Venous insufficiency is associated with old age and diabetes. Radiographic findings: if you take an x-ray, bone changes will be related to the periosteam. Usually there will be a thick, undulating periosteal response which is most commonly in the lower limbs, and is believed to be related to hypoxia. All other findings should be normal. Clinical significance: diminished arterial pulses, edema, varicosities, skin discoloration, altered temperature, varicose veins, trophic changes (ulcers, gangrenous changes).

Nutritional, Metabolic and Endocrine Diseases

Osteoporosis
Osteoporosis is defined as a decreased amount of normal bone, which is usually age- related. It can be steroid induced (corticosteroids) or heparin induced. It can also be secondary to hyperthyroidism. Senile/Postmenopausal Osteoporosis Increased patient age results in generalized osteoporosis of the whole skeleton. It th th usually presents in the 5 and 6 decades of life. There is a 4F:1M ratio. Bone quality will be normal, but there will be a deficient amount of bone. Radiographic findings: Increased bone radiolucency, cortical and medullary bone resorption resulting in thinned cortices and trabecular attenuation. Clinical Significance: pain only if associated fracture or deformity. No laboratory findings.

Heavy Metal Poisoning

Ingestion of lead pain/fumes from burning storage batteries. Most common cause is from ingestion of lead, phosphorous, bismuth, aluminum, or copper. 95% of the lead will deposit in the bone and dentine. Radiographic findings: The hallmark are dense transverse metaphyseal lines, AKA lead lines. Remodeling abnormalities.

Regional Osteoporosis
Regional osteoporosis is when there is osteoporosis only at one region, not throughout the entire body. There are three types of regional osteoporosis: reflex sympathetic dystrophy syndrome (AKA complex regional pain syndrome), disuse and immobilization osteoporosis, and transient regional osteoporosis.

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Clinical Significance: abdominal pain, encephalopathy, disturbance of nervous system, adverse effects of the lungs, blood vessels, testes, sperm, liver and brain with lead exposure. Clinical Significance: laboratory findings for primary HPTH include hypercalcemia, phosphatase. Lab tests for secondary HPTH include loss of calcium, phosphorus, parathyroid gland releasing hormones, serum calcium levels low, and PTH levels are increased. The patient will present with weakness and lethargy.

49

Rickets
Rickets can occur from a Vitamin D deficiency or malabsorption syndrome, lack of sun exposure to UV radiation, metabolic defects, chronic acidosis, renal tubular defects, aluminum intoxication, chronic administration of anticonvulsants in children. Abnormal uncalcified osteoid bone. In adults, this condition is called Osteomalacia. Radiographic findings: the bone will appear osteopenic, soft and the metaphysis becomes cupped and frayed (Paintbrush metaphysis). Occurs in weight bearing bones, trabecular changes, wide growth plates, bowing deformities, fractures, decreased bony length, scoliosis and pseudofractures. Clinical significance: bones may be tender to touch.

Scurvy
AKA Barlows Disease, which is a vitamin C deficiency usually in children 8-14 months (usually in children fed solely on pasteurized milk). Radiographic findings: Osteopenia, wimburgers sign (ring epiphysis/white band around the epiphysis), white line of frankel (white line around metaphysis), trummerfeld zone (lucent band under metaphysis), pelkins fracture (bone spurs coming off metaphyseal margins at 90 angles from shaft axis. Clinical Significance: takes 4-10 months to develop, and is prone to spontaneous hemorrhaging in areas where you get swelling, painful, irritable to touch.

Osteomalacia
This is the softening of existing bone from a lack of osteoid mineralization from a lack of intake, low absorption, or renal disease. Radiographic findings: decreased bone density with coarse trabecular patterns, loss of cortical definition, pseudofractures and deformities. No metaphyseal involvement in adults. Pseudofractures. Loosers Lines. Clinical Significance: muscle weakness, bone pain, deformities, elevated parathyroid hormone, alkaline phosphatase, hydroxyproline, normal to decreased calcium and phosphorous.

Acromegaly
Acromegaly arises from a pituitary adenoma causing an overproduction of GH (growth hormone) (after the growth plates have fused). If the patient has an overproduction of GH before skeletal maturity, the resulting condition is termed gigantism, because the whole body will be affected (and will be larger than normal). If a patient has an overproduction of GH after skeletal maturity, the resulting condition is acromegaly. Radiographic findings: Overgrowth of bones, sinuses and soft tissues. Thickened diaphysis, articular cartilage expansion. Wide joint spaces (initially) with spade-like distal tufts. Sella turcica enlargement, sinus overgrowth, malocclusion. Wide disc/facet spaces, posterior vertebral body scalloping, wide atlanto-dental interspace in the spine. Increased heel fat pad thickness (normally 2 cm). Renal osteodystrophy (linear st nd calcifications) between 1 and 2 digits. Clinical Significance: malocclusion, prominent forehead, thick tongue and thick skin on the hand.

Hyperparathyroidism
HPTH can be primary, secondary or tertiary. Primary HPTH is due to a problem with the parathyroid gland (such as a tumor), or too much PTH secretion causing increased osteoclastic activity. Secondary HPTH can be due to renal disease, and tertiary can occur in patients on dialysis. HPTH occurs in F3:M1, in patients aged 30-50 YOA. There will be osteoclastic and osteocytic resorption with fibrous tissue replacement. Radiographic findings: the hallmark for HPTH is subperiosteal bone resorption. There will also be generalized osteopenia, subchondral resorption, brown tumors, (from hemorrhagic giant cell proliferations), loss of cortical definition. HPTH targets the hands (distal tufts, middle and proximal phalanges). The skull and spine can also be affected. Osteopenia, trabecular accentuation, endplate concavities, rugger jersey spine, wide SI joints, loss of endplates, vertebral body destruction and decreased disc height can all occur.

Diabetes
Radiographic findings: Vascular calcifications between the first and second metatarsal, most commonly.

Trauma
Plain film radiography is helpful for trauma because it is cost effective, timely, and allows for a rapid initial evaluation. However, it can be difficult to see small bony fragments,

 soft tissue pathology, and complicated fracture patterns. The ACCR Guidelines for Plain Film Radiology suggest that the need for radiographic examination is based on the history and physical examination. You must ask yourself if the benefits of radiographic examination are greater than the risk of ionizing radiation? Radiography can be used to diagnose, identify contraindications to Chiropractic care, identify bone and joint morphology, acquire postural/kinematic/biomechanical information. Routine radiography as a screening procedure is not appropriate except under public health guidelines. Advanced imaging has its benefits because it allows for 3D visualization. CT allows for more osseous visualization, but it does not substitute for plain film examination. It is an important adjunctive procedure in diagnosing and evaluating trauma. Indications for CT include: if the patients plain films suggest or show a fracture of the vertebral body, if there is a disagreement between neurological and radiological findings, and if the patient suffered from acute head trauma. The reliability of emergency room physicians at interpreting trauma radiographs is interesting. Most Junior Doctors misdiagnosed significant trauma abnormalities on x- ray, and the Senior Doctors scored higher, but were not infallible. Interprofessional comparison indicated that Chiropractic Radiologists scored the highest . Clinical evaluation of a fracture patient may include findings such as a visible or palpable deformity, local swelling, visible ecchymosis, local tenderness over the bone, impairment of function, abnormal mobility (movement between fragments), and crepitus with motion. Always check circulation and sensation distal to the injury, and of all involved parts! To make a diagnosis, you must have at least 2 views of the bone involved, at 90 to each other. You must include both adjacent joints. In kids, comparison views (side to side) are often helpful. How to describe a fracture: You must note you ABCS! Alignment of bones and fracture fragments (look to the roentgenometrics). Look at the Bones; their cortices, medullary bones, if you see areas of lucency or density, callus formation, the periostem, the boney fragments, cortices surrounding the fragments, etc. Cartilage is also important to look at. Is there any joint involvement or intraarticular fracture? Is the Soft tissue swollen (immediate fracture) or not (old/healed fracture)? If you dont see anything at first, then look to the soft tissues that will help you to locate where the problem is. Fractures & Dislocations Fractures involve a complete disruption in the continuity of a bone (simple or comminuted. Failure of a structure due to excessive loading and energy absorption. A simple fracture occurs when there is one fracture site and two fragments arising from it.

50 A comminuted fracture occurs when the bone splits into multiple pieces. There will be more than 2 resulting fracture pieces. Incomplete fracture = Some of the bony trabeculae are completely severed, others are bent or remain intact (kids). Dislocation = A complete disruption of a joint; articular surfaces are no longer intact. Subluxation (medical) = A minor disruption of a joint; articular surfaces are no longer intact. Closed Fracture = The bone does not pierce through the skin. Open Fracture = The fractured bone pierces through the skin. Stress/Fatigue Fracture = Fracture from chronic use. Occult Fracture = There is clinical suspicion of a fracture, but the fracture is not radiographically present and you may need to re-take the x-rays. Common in elderly along with scaphoid fractures. Stable Fractures = A fracture that does not move, or is unlikely to move during healing. There is little probability of producing neurological compromise. Unstable Fracture = A fracture that does move, and is neurologically unstable. Avulsion Fracture = Involves the site of attachment of tendons/ligaments, and when these structures pull a piece of bone off. Impaction/Depressed/Compression Fracture = Telescoping of the trabeculations on top of each other. One part of the bone is driven into another, possibly causing shortening of the bone. Most common in the femoral neck. Depression Fracture = A depressed surface, change in the outer cortical margin as it bulges inwards (M/C tibial plateau, or the frontal bone in the skull). Compression Fracture = When the overall size of the bone becomes decreased (in the spine and calcaneus only). Incomplete (Pediatric) Fracture = When a fracture does not extend the whole way through the bone. The bone is broken only on one side of the bone. There may be buckling or bending on one side of the bone, and this can be the only sign of fracture. There are three types of pediatric fractures: torus/buckling fractures, greenstick/hickory stick fractures, and bowing fractures. Torus/Buckling Fractures occur from compressive forces causing the cortex to bow outwards, usually in the metaphyseal region. You will see a little blip in the cortical margins. In greenstick/hickory stick fracture (kids <10

RADIOLOGY REVIEW
years old), one side of the bone will remain intact, but the other surface will be bent. Bending of the bone applies tension to the cortex side of the bone and a transverse fracture on the convexity with the concave side remaining intact. Most heal without complications. Bowing fractures present as acute plastic bowing. Complete Fracture = Occurs when the fracture goes all the way through the bone (this is the most common presentation). Chip (Corner) Fracture = This is a type of avulsion fracture that involves the corner of a bone (for example, the base of a distal phalanx, making it look like an avulsion fracture). Pathological Fracture = A fracture through a bone that is weakened by a localized or systemic disease process. Usually a transverse fracture and often seem quite smooth. Stress/Fatigue Fracture = A fracture from repetitive stress which causes microfractures which eventually leads to a fracture. A stress fracture through a diseased bone is called an insufficiency fracture. Pseudofracture = This is not a true fracture. It represents an insufficiency fracture or from vascular pulsations. You will see a linear lucency on the convex surface of the bone. Often multiple, and can be associated with bone-softening conditions such as Pagets, Rickets, Osteomalacia, and Fibrous Dysplasia. Different synonyms applied such as Loosers Lines, Milkmans Syndrome, Increment Fracture, and Umbau Zonen. Evaluating Fractures: You must detail the anatomic site of trauma, extent of the fracture (how far along the bone it is), type of fracture (complete/incomplete), alignment of the fragments (displacement, angulation, rotation, foreshortening, distraction), direction in relation to the longitudinal axis of the bone, special features (impaction, depression, compression), associated abnormalities (dislocation, diastasis), special type of fracture (pathological), or if it is an open/compound or closed/simple fracture. Classification of Fractures: Fractures can be classified into three different types; those caused solely by sudden injury (which is most common), fatigue, insufficiency (normal stress on abnormal bone), or stress fractures (abnormal stress placed on normal bone), or pathological fractures. The orientation of the fracture can be oblique (45 to the long axis of the bone shaft), spiral (torsion in mechanism, sharp ends of bone), transverse (usually associated with pathological bone, for example in Pagetoid bone), or Longitudinal fractures (which fracture along the length of the bone. Spatial relationships that must be nodded include alignment, angulation, apposition, and rotation. Alignment refers to the position of the distal segment in relation to the proximal segment. Angulation refers to the angle made by the long axis of the fracture

51 fragments. Apposition refers to the closeness of opposing surfaces of the fractures and rotation refers to twisting along the long axis of the bone. How to determine the age of a fracture = If the fracture is new, you will see soft tissue swelling and sharp fracture edges. If the fracture is recent (but not new), the soft tissue swelling will have disappeared, and you will start to see blunting of the fracture edges. The fracture line will be wider. In a healing fracture, you will see callus formation, which will appear as fluffy, cloud-like calcific densities. An old and well-healed fracture will appear as remodeled bone. In the spine, a new or recent fracture will appear with a step defect and/or a zone of sclerosis, with paraspinal soft tissue swelling. An older fracture will present with a wedge deformity without any other signs. Fracture repair process = There are three phases of bone tissue repair. The first phase is the circulatory or inflammatory phase, which typically lasts 30 days. The first 10 days are known as the Cellular phase where there is inflammation, and a cellular response is prominent in the first five days (cell death). You will have a lot of granulation tissue. From days 10-20 the vascular phase takes over, when there will be an open capillary network around the fracture site. The periosteum will be deviated and responds. The primary callus will form. From days 20-30, the primary callus phase is evident. Vasculature will be well-established, raw minerals will be available, and this is the earliest point in which you will see the callus on x-ray (14 days). The second phase of fracture repair is the reparative or metabolic phase. You will see orderly secretion of the callus, removal of osteoid to be replaced by mature bone, sealing, buttressing, bridging, uniting, and clinical healing is achieved during this phase. The third phase of fracture healing is the remodeling or mechanical phase. This phase involves realigning and remodeling of bone according to Wolfes Law, and restoration of marrow to marrow cavity. This phase can last years. Rate of fracture union = The time for a fracture to unite is variable. In young children the union will be more rapid. The callus will be visible in about 2 weeks, with bone consolidation occurring within 4-6 weeks. In older children, the process is slower than this. In adults, fractures of long bones in favorable conditions heal in 3 months, but may extend for 4-5 months. Complications of fractures = Include delayed union (clinical diagnosis), non-union (x-ray diagnosis, rounded fractured ends with cortical bone), mal-union (healed in unacceptable position), AVN, complex regional pain syndrome (Sudecks atrophy, causalgia, reflex sympathetic dystrophy), infection, traumatic arthritis, or disuse osteoporosis.

 Immediate complications of fractures include arterial injuries. The most common site of arterial injury is the popliteal artery, superficial femoral artery, brachial artery (elbow fracture), aortic arch (sternal fracture), iliac arteries (pelvic fracture), or the axillary artery (shoulder dislocation). Compartment syndromes (i.e. Volkmanns ischemic contracture) can occur, where there is an increase in the pressure in a closed compartment from hemorrhage and edema. The anterior tibial and anterior forearm compartment are commonly affected. Gas gangrene may occur in 1-3 days in the buttock or thighs. Fat emoblisms may present in major bones. 50% of fat emboli have multiple fractures, 30% occurring from the femur alone, 5% in the pelvis and small bones. Having a bedridden patient is a risk for fat emboli. Osteomyelitis can occur in 15% of open fractures, commonly from S. Aureus, more common in the femur than the tibia. Hardware failure can occur, complex regional pain syndrome, post-traumatic osteolysis (most common in the AC joint and pubic bones), re-fracture, myositis ossificans, synostosis, or delayed union can occur. Delayed complications include osteonecrosis of the femoral or humeral head, scaphoid or talus, DJD, arthropathy and toxicity, disuse osteoporosis, ABCs, malunion, or nonunion. Cervical Spine Trauma Instability on a lateral cervical spine film will include 3.5 mm horizontal translation of one vertebral segment over another, or 11 degrees or more of angular deformity between 2 adjacent vertebral segments. Steeles Rule of Thirds = 1/3 of the ring of the atlas is needed for the spinal cord, odontoid process and the last 1/3 is free space. CT is very good for evaluating fractures in the cervical spine. The thinnest possible contiguous slices should be used (2-3 mm), with 1-1.5 mm for dens fractures. Reformatting still required to help pick some fractures up. The only downside of CT is that ligamentous or soft tissue injuries are not shown. MRI is better than CT in diagnosing the presence of extent of an acute epidural mass. There are three columns that need to be evaluated when looking at the cervical lateral view. The posterior column is the spinolaminar line, the middle columns is along the posterior vertebral bodies/Georges Line, and the anterior column is along the anterior vertebral bodies. If two or more of the above columns are disrupted, the cervical spine can be classified as unstable. You may also see acute kyphosis (hyperflexed segment), gapping of the facets, and/or fanning of the spinous processes. If you determine a fracture is unstable, collar and hollar! Signs of instability on the neutral lateral view = include acute focal kyphosis, disruption of Georges line, disruption of the posterior cervical line, gapping of the facet joints, and fanning of the spinous processes.

52 Indications to do flexion/extension lateral cervical radiographs = not initially required until a 3 view series are thoroughly scrutinized. With CT and MRI, flexion/extension views will become obsolete. How to differentiate between an avulsion fracture of the spinous process and an unfused apophysis = a new fracture has sharp margins with an open marrow cavity, and an old fracture has smooth cortical bone surrounding both sides of the fracture line. In an avulsion fracture the displaced segment will have moved inferiorly, while the unfused apophysis will line with up the rest of the spinous! MRI = Standard screenings include a sagittal T1 and T2, and no reformatting is required. T2 is best for evaluating the central canal. Fat suppression techniques are excellent for trauma because they will show the edema! MRI may be unnecessary in acute phased whiplash patients due to high false positive results. Thoracic and Lumbar Trauma 51% of all injuries outside the cervical spine occur at the thoracolumbar junction. Anatomic features can predispose a patient to thoracolumbar junction injuries, such as the change from a kyphotic to lordotic alignment, loss of stability provided by the ribs, increased mobility compared to the upper thoracic spine, and the change in facet orientation. Stability in the thoracic spine = Similar to the cervical spine, assess the quality of the three columns. If one columns is involved/abnormal, the injury is likely stable. If two columns are involved, the injury is likely unstable, and if all three columns are involved, the injury is unstable. Instability is also suggested if there is a fracture dislocation, post- traumatic kyphosis >40, sternal or rib fractures, or costovertebral dislocation. Indirect signs of thoracic spine injury include: paravertebral hematoma, mediastinal widening, pleural fluid (hemothorax), sternal fractures, rib fractures and costovertebral dislocation, or double spinous process sign. Indications for Radiography in patients with thoracolumbar trauma: The data suggests that patient who are awake, alert and have no clinical evidence of injury do not require radiological studies of the thoracolumbar spine. Patients with equivocal or positive clinical findings or with altered level of consciousness should have a complete thoracolumbar spine evaluation. There are four classifications of thoracolumbar injuries: compression fractures, burst fractures, seat belt (chancre) fractures and fracture dislocations. Adynamic Ileus is a temporary loss of peristalsis in the gut. If the patient presents with adynamic ileus, this suggests that there is a fracture present, especially in acute trauma cases! The somatovisceral reflex will be affected, causing a marked loss of bowel sounds, distension, nausea and vomiting.

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Burst fractures are usually due to vertical compression, and must be stable if there is no damage to the posterior elements. Late neurological deficits occur in 20% of cases. CT or MRI are the best was to assess for burst fractures. The two most common causes of pathological fractures in the elderly are mets and myeloma. Sacral Trauma A normal scan of the sacrum will show symmetric uptake of radiographic material, accumulation in the bladder, kidneys and urethra, and normal joint uptake. In trauma cases, bone scans are relatively not specific, with a delay in uptake at the trauma site (damaged vasculature prevents distribution of radiographic material). Remains positive for variable lengths of time. Knee Trauma FBI Sign = Fat, Blood, Interface, suggests an intra-articular fracture. Fat escapes from bone marrow because the fracture into the joint and floats to the top of synovial fluid mixed with blood. Helps to determine occult fractures.

53 occur in the distal tibia, proximal tibia, or distal femur. Type IV S-H fractures occur through the metaphysis and epiphysis, crossing the physis. Type IVs make up 10% of all epiphyseal fracture and have a poor prognosis, occur with associated growth disturbances, and requires open reduction. S-H Type V is when there is compression of the physis, and make up only 1% of fractures of the physis. Type Vs have a poor prognosis, and commonly occur in 12-16 year olds. Deformity is common in Type V S-H fractures.

Myositis Ossificans
Myositis ossificans is a heterotropic ossification occurring in damaged tissues, associated with hemorrhaging and bruising. Radiographic findings: The most common sites of myositis ossificans include the elbow (brachialis), thigh (quads), knee (Pellegrini-Stieda), deltoid, adductor magnus (Prussians disease), psoas (lumbar ossified bridge), ischial tuberosities (bedridden or wheel chair bound), paravertebral ossification (paraplegia, quadriplegia). Achilles tendon (post surgery), cortical irregularity is common (posterior distal femur). Clinical Significance: there are three stages to the generation of myositis ossificans. Stage one involves the development of a pseudosarcoma (metaplastic bone formation following injury), and usually lasts 15-30 days unless re-injured. If biopsied, it will be interpreted as osteosarcoma. Clinical history is KEY. In the early stages, all you will see is soft tissue swelling, then the bone forms. Stage 2 involves differentiation. This occurs nd rd in the 2 -3 months. There will be a zoning phenomenon (peripheral organization, central lucency. Cleavage plane (lucency between ossification of soft tissues and bone). Stage 3 involves maturation, shrinkage, resolves/resorbes or further organizes. Periosteum develops and can now be surgically removed. You must rule out aggressive lesions (parosteal osteosarcoma). Once the lesion is matured, then it can be removed, but until this point they will not.

Stress Fractures
There are different types of stress fractures: fatigue and insufficiency fractures. Fatigue fractures occur when ABNORMAL stress is placed on NORMAL bones. Insufficiency fractures occur when NORMAL stresses are placed on ABNORMAL bones. It is most common in C5-7, in 75% of patients. Neurological problems and instability issues are important to address. Radiographic findings: Fatigue fractures are common at the 2 and 3 metatarsals (March fractures, Deutchlanders fracture), proximal tibial fractures, fibula (proximal or distal) fractures, pars interarticularis fractures, femoral neck fractures, among others. Periosteal response, periosteal/endosteal thickening, fracture lines, transverse opaque bands. Clinical significance: DDx: osteomyelitis, osteosarcoma, osteoid osteoma, or growth arrest lines.
nd rd

Jefferson Fracture (Burst Fracture of C1)

Fracture through the posterior or anterior arch of C1. Due to vertical compression, encouraging lateral displacement of the atlantal masses. Radiographic findings: Total overhang or offset >7 mm indicates a fracture. Atlantodental interval >3 mm in adult suggests instability. On the APOM the lateral borders of C1 will be wider than the border of C2, overhand. Parodontal spaces will also be large. Common in C5-7 region. Clinical Significance: spinal cord compression is rare. Retropharyngeal hemorrhage and delayed instability are major concerns. May be stable if no damage to the posterior element occurs. A stable Jefferson fracture manifests an intact transverse ligament. An

Growth Plate Injuries/Salter-Harris-Epiphyseal Injuries

There are five types of Salter-Harris fractures. Type I Salter-Harris fractures occur through the physis, and are difficult to see if not significantly displaced. Make up 6% of epiphyseal injuries (ex: SCFE). S-H Type II fractures occur through the physis and metaphysis, making up 75% of all physis injuries. Type II fractures commonly occur in the distal radius, tibia, fibula, femur and ulna. You will see the Thurston Holland fragment sign. In Type III S-H fractures, the fracture will go through the physis and epiphysis, making up 8% of all physis injuries. These occur in 10-15 year olds, and like to

 unstable Jefferson fracture has a disrupted transverse ligament. Late neurological changes in 20% of cases. Advanced imaging such as CT or MRI is critical in assessing possible adverse effects on the cord, vertebral canal for osseous fragments of epidural mass. Note: Pseudospread of C1 in kids under 6 years of age, will have developmental clefts of C1 (offset <2 mm).

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Unilateral Locked Facets

When one facet jumps off its corresponding facet, and the other stays in tact with its corresponding facet. Radiographic findings: Anterolisthesis and evidence of rotation (pillars not superimposed, you will see the iVF or Bow Tie Sign). Anterior vertebral body line is disrupted, Georges line is disrupted, with unilateral locking or perching of facets is common. Tomography may provide additional information for a complete evaluation of the degree of dislocation. Clinical significance: hyperflexion and rotation injuries. This is a stable injury. PLL, interspinous ligaments, facet capsules and IVDs are often injured. Neurological damages may be significant.

Odontoid Fracture
There are three classifications of odontoid fractures, Type I, II and III. Type I involves an oblique fracture limited to the superior one half of the dens. Type II odontoid fractures involve a transverse fracture at the base of the dens. Type III odontoid fractures involve the base of the dens and extend into the body of C2. Clinical significance: there is a high incidence of nonunion with type II odontoid fractures. Patients are more likely to fracture the dens than rupture the transverse ligament.

Bilateral Locked Facets

When the superior and inferior facets no longer touching their respective facet pairs. Radiographic findings: anterior and posterior vertebral body alignment disrupted. Clinical Significance: Unilateral locking or perching of the facets is common. Tomography may provide additional information for more complete evaluation of the degree of dislocation. The PLL, interspinous ligaments, facet capsules and IVDs are often injured or disrupted to various degrees. Neurologic damage may be significant.

Hangmans Fracture
There are three classifications of Hangmans fractures. We only looked at the first type, so dont worry about types II or III. Type I involves an undisplaced fracture involving the posterior body or any part of the ring of C2. The C2-3 disc is intact. Clinical Significance: Tendency towards instability. Associated damage to ligamentous structures and cord must be considered.

Pseudosubluxation
When there is anterior translation of one vertebral body on another. Radiographic findings: if greater than 3.5 mm, this is bad news.

Flexion-Type Teardrop Fracture

This is a hyperflexion type injury, and is considered highly unstable, neurological involvement such as quadriplegia is present in a high percentage of patients. IVD damage is common. Anterior inferior corner of the vertebral body will be displaced. Radiographic findings: Look at Georges line for disruption, bony fragments displaced off the vertebral bodies, soft tissue swelling horizontal displacement, usually between C4-7. Clinical Significance: highly unstable, neurological involvement such as quadriplegia is present in 87% of patients. IVD damage is common. These fractures are unstable. Do not confuse a tear drop fracture with an intercalary bone or limbus bones! Look for the continuous cortical margins around the vertebral body and cortical bone around the bony fragment. Is there soft tissue swelling?

Chance Fracture
Combination of flexion and distraction forces cause this fracture. The seat belt will cause an anterior fulcrum close to the spine. Posterior arch goes undetected in many cases.

Lumbar Ossified Bridge Syndrome (LOBS)

Myositis ossificans from one TVP to the adjacent TVP on the same side.

Traumatic Syringohydromyelia
Etiologies include trauma, arachnoiditis, degenerative disease/intramedulary neoplasms.

Clinical significance: must differentiate from cord tumors. MRI extremely effective in demonstrating syrinx formation. Possibility of cord tumor must be considered when a This involves trauma to the cord, which could lead to inflammation within the cord itself. syrinx is encountered.

Post-Traumatic Cord Myelomalacia

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55 Radiographic findings: Best seen on CT. Clinical significance: May cause pressure on the anterior part of the spinal cord causing neurological deficit/paralysis.

Posterior Apophyseal Ring Fracture

Separation of the posterior vertebral body ring apophysis. Limbus Bone. Weakness between the osteocartilaginous junction between the apophysis and the vertebral body. These fractures can result from trauma (MVA, weight lifting, sports or gymnastics). Clinical Significance: most common in adolescents and young adults. The patient will have stiffness and spasm, numbness, weakness, neurologic claudication, possibly cauda equina syndrome.

Sacral Fractures
Sacral fractures occur from a fall on the buttocks (causing a horizontal fracture) or indirect trauma to the sacrum (blow to a flexed femur). There are two types of sacral fractures, horizontal and vertical fractures. Horizontal fracture (arcuate line) are best seen in the lateral view. Vertical fractures are associated with organ damage in 50% of cases. Check the anterior sacral foramina and the rest of the pelvic ring. There are two types of ring fractures: Malgaignes Fracture, and Bucket Handle Fractures. The two types of pelvic dislocations are sprung pelvis and pubic diastasis.

TVP Fractures
Radiographic findings: Often many TVPs will fracture in a row, and are usually unilateral. Clinical significance: must do a UA (urine analysis). Prone to non-union. If TVP L5 is fractured, you must check the entire pelvis for fractures and dislocations.

Sternal Fractures
Fractures to the sternum are usually due to trauma (MVA with no seatbelt and the persons chest hits the stearing wheel). Clinical significance: 40% of people with sternal fractures die from damage to underlying important structures. Always check for post-traumatic aortic aneurysm.

Malgaignes Fracture
This is if there is an ipsilateral double vertical fracture of the inferior ring and SIJ. Malgaignes fracture is the most common pelvic fracture. This is an unstable fracture.

Bucket Handle Fracture

The bucket handle fracture is a ramus fracture with contralateral SI involvement. This type of fracture is associated with severe trauma and other injuries. This is an unstable fracture.

Rib Fractures
Radiographic findings: rib fractures generally occur in a row, and are often occult (cant see). You may need to re-x-ray 5-7 days later. Clinical significance: You must rule out pneumothorax. If ribs are fractured in more than one place on the same rib, the patient could develop flail chest. The patient would need a respirator. Generally ribs will heal by themselves.

Sprung Pelvis
This is a severe, pubic diastasis with one or both SI joint diastasis. This is an unstable fracture.

Pubic Diastasis
The width of the pubic symphysis should not exceed 10 mm in non-pregnant women; dont overlook unilateral SI diastasis.

Wedge Fractures
Occurs as a result of mechanical compression of the involved vertebra between the adjacent vertebral bodies, from forced hyperflexion. Radiographic findings: common at C5, 6 and 7. Clinical significance: These are stable fractures.

Straddle Fracture
This is a fracture through the anterior rami on both sides. This is an unstable fracture. The bladder sits right above this so it is often affected.

Coccyx Fracture
The coccyx will fracture transversely. This is difficult to diagnose! You cannot make your diagnosis relying on coccyx position.

Burst Fractures
Vertical compression to the head propelling, causing the nucleus pulposus through the endplate into the vertebral body. The force causes the vertebral body to fracture vertically.

Iliac Wing Fracture

AKA Duvernys Fracture (which is stable). ASIS will be affected in gymnasts, hurdlers, cheerleaders. AIIS can be affected in rugby, soccer, football.

56 Clinical significance: Extracapular hip fractures are usually pathological. Look for extra density surrounding the fracture line which is often due to compaction.

Hip Dislocations
Hips can be dislocated superiorly, anteriorly or centrally. Clinical significance: Complications of hip dislocations include sciatic nerve palsy (15%), myositis ossificans, AVN, and DJD. If a child presents to you with a constant/intermittent hip pain, you need to rule out SCFE!! If you do find SCFE, orthopedic referral is required!!

Avulsion Fracture
An avulsion fracture is when a muscle pulls a piece of bone off of the major bone. Radiographic findings: You should see a fragment of bone that is well corticated on two sides, and fragmented on the other. Mention the displacement of the fragment when describing this fracture (where did it go in relationship to where it came from?) Muscle attachment sites where avulsion fractures commonly occur: greater trochanter (gluteal muscles attachment), ischial tuberosity (hamstrings), symphysis pubis (adductors), ASIS (Sartorius), AIIS (rectus femoris), and lesser trochanter (psoas). Clinical significance: This is a stable fracture.

Posterior Hip Dislocation

Posterior hip dislocations occur from a blow to the knee/foot while the hip is flexed (driving force through femur). This is the most common dislocation in the hip. Radiographic findings: The femoral head is displaced superiorly. Clinical significance: often associated with small femoral head fractures (13%), posterior rim fractures (90%), acetabular fractures, and femoral shaft fractures.

Hip Trauma
There is a 2:1 female to male ratio. Up to 20% of hip fractures are not detected within 24 hours of injury. Usually in osteoporotic patients. Radiographic findings: bone scans and MRI are great at detecting subtle fractures. Clinical significance: There is a high risk for thromboembolic disease. This is a very costly type of injury.

Anterior Hip Dislocation

Anterior hip dislocations occur from forced abduction and femoral extension. Radiographic findings: the femoral head will be displaced inferiorly. The femoral head overlies the obturator foramen with this dislocation. Clinical significance: Anterior hip dislocations are associated with fractures of the femoral head and acetabular rim.

Intracapsular Hip Fractures

Radiographic Findings: Occur in the femoral neck, and there are three types: subcapital, midcervical, and basicervical. Subcapital fractures occur at the superior part of the femoral neck, and usually come from an impaction etiology. Midcervical fractures are uncommon. Basicervical fractures occur at the inferior most part of the femoral neck, and are uncommon. Clinical significance: A common complication of an intracapsular hip fracture is AVN/non-union.

Central Hip Dislocation

Central hip dislocations occur from a blow to the lateral side of the body. The femoral head is pushed into the pelvis, and the acetabulum fractures and is forced axially through the pelvis. Radiographic findings: The femoral head may lie inside the pelvis. Clinical significance: associated with acetabulur fracture.

Extracapsular Hip Fractures

Radiographic findings: There are three types of extracapsular hip fractures: trochanter, intertrochanteric or subtrochanteric. Trochanteric fractures occur through the greater trochanter only. Intertrochanteric fractures extend from the greater trochanter through the femur towards and through the lesser trochanter. Subtrochanteric fractures occur at the surgical neck of the femur.

Supracondylar Fracture (Distal Femur)

This is a fracture through the supracondylar area distal to the femoral shaft and proximal to the condyles. Radiographic findings: this can be a transverse/oblique fracture which is often comminuted and intraarticular.

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Clinical significance: This type of fracture is associated with hip dislocations. When you have a supracondylar fracture and a tibial fracture, this is called a floating knee.

57 Clinical significance: These fractures are usually associated with ligament and capsular damage, and plateau fractures. The common peroneal nerve can be damaged. Adduction injuries causing peroneal nerve injuries can cause rupture of the lateral capsular and ligaments, which are called lateral compartment syndrome of the knee, and ligamentous peroneal nerve syndrome.

Femoral Condylar Fracture

Radiographic Findings: This fracture can be T or Y shaped, and it is always intra-articular. It is confined to one condyle, and the fracture is usually oblique. It may result in an intra-articular loose body. Clinical significance: Femoral condylar fractures can lead to osteochondral defects, and commonly leads to joint deformity.

Patellar Fractures
Radiographic findings: Patellar fractures can be transverse (60%), comminuted (25%) or vertical (15%).

Tibial Plateau (Bumper or Fender Fracture)

Tibial plateau fractures are from MVAs 25% of the time. Radiographic findings: 80% of the time, the lateral plateau is fractures alone, and only a few percent involve both plateaus. Fewer still involve the medial tibial plateau only. You will see depression of the lateral tibial joint surface with or without a vertical radiolucent line through the joint surface. Clinical significance: 50% of the time, these fractures occur in patients over 50 years of age. Associated with ligamentous damage most of the time.

Patellar Dislocation
Patellar dislocations are most commonly in the lateral direction, and are common in females. Upon relocation, a flake fracture can result. Etiology includes: volleyball, basketball or any sort of jumping sports. Radiographic findings: MRI will show underlying bone bruise in a particular pattern. Clinical significance: associated osteochondral fracture.

Femorotibial Dislocation
Femorotibial dislocations occur from severe falling injuries from a significant height. Radiographic findings: the dislocation can be either anterior or posteriorly directed. The cruciate ligaments are often torn with injuries to the popliteal artery and peroneal nerve. Stress radiography shows torn collateral ligaments.

Trampoline Fracture
These are fractures of the proximal tibia, occurring in kids who jump on a trampoline with a bigger person. When the bigger person jumps, the trampoline mat recoils up and the small kid will land on the mat (which is moving up), impacting the tibia. Radiographic findings: Fracture through the proximal tibial metaphysis. Clinical significance: common in 2-10 year olds.

Proximal Tibiofibular Dislocation

Dislocation of the proximal tibiofibular joint can be anterior, posterior or superiorly directed. Based on the displacement of the head of the fibula. Etiology: fall with crossed legs. Most commonly, the dislocation is in the anterolateral dislocation.

Segonds Fracture
Avulsion of the TFL from the tibia. Radiographic findings: You will see a small bony flake adjacent to the lateral tibial condyle. Clinical significance: 75% have associated meniscal and ACL tears.

Internal Derangement: Ligamentous Injuries

This is far more common than a fracture of dislocation! Derangement can include the collateral ligament (Pellegrini-Steida or the MCL proximally), the ACL, PCL, menisci. Radiographic findings: ACL tears are easier to tear and harder to see. PCL tears are header to tear, and easier to see. 97% of menisci problems are detected with MRI. There will be a linear high signal intensity, there are 3 grades and 7 types.

Proximal Fibular Fracture

Radiographic findings: Isolated fractures are rare. Can be impacted, comminuted, or avulsed off the proximal pole of styloid process. You can have an avulsion at the attachment of the biceps femoris or LCL.

Osgood Schlatters
This is a common avulsion type injury involving fragmentation of the tibial tuberosity (may be a normal variant). It involves overgrowth of the tibal tuberosity.

 Radiographic findings: This is NOT an x-ray diagnosis. Clinical significance: The patient will present with pain and swelling at the tibial tuberosity in adolescents. Worse when the patient uses/contracts his/her quads.

58 Clinical significance: Often found with tibiotalar dislocation. The patient will have externally rotated the foot, and therefore the fracture is laterally and posteriorly displaced.

Medial Malleolus Fracture

Fracture of the medial malleolus, created by angular forces by movement of the talus against the medial malleolus. Radiographic findings: Fractures are usually transverse or oblique. Best seen on the AP radiograph, will see a radiolucent line with soft tissue swelling. Clinical significance: if the fracture is distal to the plafond, the fracture is considered stable. If the fracture is more proximal, this is less stable.

Potts Fracture
This is a fibular fracture, 6-7 cm proximal to the lateral malleolus with a rupture of the distal tibiofibular ligament and partial dislocation. Etiology: jumping or leaping injury.

Dupuytrens Fracture
Dupuytrens fracture is a fracture of the distal tibia. There will be diastasis with the tibia, lateral dislocation of the talus, a torn distal tibiofibular ligament and up and out displacement of the foot.

Maisonneuves Fracture
This is a fracture of the proximal fibular shaft with rupture of the distal syndesmosis. Etiology: foreceful inversion and external rotation of the ankle.

Lateral Malleolus Fracture

When the most distal part of the fibula is fractured. The most common fracture here is a spiral fracture from the anterior inferior margin up and back to the posterior part of the shaft of the distal fibula. Etiology: external rotation of the foot. Radiographic findings: Oblique fractures are most common in the lateral malleolus. You may seen the McKenzie Sign which occurs when there is a radiolucent oblique fracture of the lateral malleolus and soft tissue swelling. You need a medial oblique projection, as a radiolucent oblique line with soft tissue swelling. You may see an avulsion fracture around the tip of the lateral malleolus, from the lateral collateral ligaments. May also see a small talar dome osteochondral fracture as well. Clinical significance: Avulsion and talar dome fractures are common.

Tillauxs Fracture
A fracture through the medial malleolus with distal syndesmosis diastatis, avulsion of the anterior tubercle of distal tibia, and fracture of the distal fibular (6-7 cm about the joint). Radiographic findings: There are three fractures involved in Tillauxs Fracture: a medial malleolar fracture, anterior tibial fracture and distal fibular shaft fracture. Best seen on AP ankle x-ray.

Toddlers Fracture
An undisplaced spiral fracture of the tibia occurring in 9 months to 3 years of age. Etiology: falling, or getting the foot caught between crib slats. Rarely involves a fracture of the fibula, in which case it will not be called a BB Fracture (BB = both bones). IN adults, this is called a boot-top fracture. Radiographic findings: seen on AP or lateral.

Bimalleolar Fracture
This is a fracture through both malleoli. Radiographic findings: A transverse fracture on one malleoli, and an oblique fracture on the other. Soft tissue swelling.

Trimalleolar Fracture
This is also known as Cottons Fracture, and involves the medial and lateral malleoli, as well as the posterior lip of the tibia (some people the posterior tip of the tibia the third malleolus). Radiographic findings: Includes the posterior process or lip of the tibia, the lateral and medial malleoli. Best seen on the lateral view.

Talar Dislocations
This is a rare dislocation, and it can occur at 1, 2 or 3 joints. Radiographic findings: in an anterior talar dislocation, all ligaments will be torn, and the dorsalis pedis pulse may be lost. In a posterior talar dislocation, surgical repair is optional.

Calcaneus Fractures/Calcaneal Compression

This is the most common tarsal fracture. 25% involve processes, and 75% involve the body of the calcaneus and the subtalar joint. Calcaneal compression occurs bilaterally in

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10% of cases, and 10% are associated with vertebral body fractures, and they can be comminuted with a tendon rupture. Radiographic findings: Boehlers angle >28 indicates calcaneus compression (involves the subtalar joint). Clinical significance: Can be associated with vertebral body fractures, especially around the thoracolumbar junction. Crush Fracture Occurs when you drop a heavy object on the phalanges. Bedroom Fracture Occurs when you stub your toe into the bed post. Chip Fracture Small fracture of the phalangeal articular margin which can follow hyperextension or hyperflexion. Hallux Rigidus st A fracture of the hallux phalanx can cause a stiff 1 MTP joint and premature DJD. Sesamoid Fractures Fractured commonly in jumpers, dancers, and runners. Most common medially.

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Talus Fractures
Radiographic findings: A fracture through the body of the talus (transverse of oblique), the dome of the talus (osteochondral fracture at the lateral or medial dome), or a fracture through the neck of the talus (Aviators astagalus, MVA). A fracture through the head is rare, and will fracture well forward of the talar neck. Clinical significance: Fracture through the neck of the talus frequently goes through AVN.

Midtarsal Chopart's Dislocations

This is a rare separation between the talonavicular and calcaneonavicular joint.

Navicular Fracture
An avulsion of the dorsal surface is most common.

Tarsometatarsal Lisfracs Dislocation

This is a rare separation of the tarso-metatarsal joints. Dorsal (and often lateral) dislocation of the metatarsal bases, with fractures at various locations along the site of dislocation. Radiographic findings: There will be too much gapping in between the 2 and 3 metatarsals at the junction of the tarsals and metatarsals. Clinical significance: common in diabetics, equestrian activities and MVAs.
nd rd

Cuneiform Fracture
Is an isolated fracture of the cuneiform is rare.

Cuboid Fracture
An isolated cuboid fracture is rare, but if it does occur, it most commonly fractures on the lateral margin. Radiographic findings: may need a bone scan for kids.

Metatarsals Fracture, the Jones (Dancers) Fracture

Osteochondritis Dissecans
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Jones/Dancers fractures are common fractures occurring at the base of the 5 metatarsal, and are usually transverse fractures 15-20 mm from the base. The most common etiology is dropping heavy objects on the metatarsals, but can also occur with plantarflexion and inversion of the foot. Remember: an apophysis is a VERTICAL lucency in the base of the 5 , if its a fracture, the lucency will by TRANSVERSE.
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Osteochondritis dissecans targets the femoral condyles, talus (medial talar dome most commonly), the hip, patella, foot (metatarsal heads), shoulder, elbow (capitellum), wrist and TMJ. The most commonly targets the talus and medial condyle. The etiology is unknown. Age of onset if between 11-20 years of age.

Labral Tears
Labral tears is described by their arthroscopic appearance, including a flap tear, buckey bandle tear, split non-detached tear, degenerative lesions and SLAP lesions. Radiographic findings: radiography, tomography, fluoscopy, contrast arthrography, CT, MRI or MR arthrography. MRI is best for bones and ST, but less effective in the superior region, and unreliable in the inferior and posterior labrum region. Arthropathy is the gold standard for diagnosing the lesion and instability.

Phalangeal Fractures
Phalangeal fractures heal on their own and do not require stabilization. These are common and include crush fractures, bedroom fractures, chip fractures, hallux rigidus and sesamoid fractures.

Rotator Cuff Tears

Acute RC tears are less common, and are activity related. Chronic RC tears are very common! Radiographic findings: The humeral head will move superiorly and there will be a decreased acromio-humeral space. May see the greater tuberosity flatten and become irregular from wear and tear. Clinical significance: 90% of people over the age of 70 have chronic RC tears!

Tendinitis and Bursitis

Tendinitis is AKA Tenosynovitis, which is an accumulation of fluid within the tendon sheath or tendon itself. Incomplete tears with degenerative changes. Burisitis is when fluid accumulates within the bursa, and can result in calcific bursitis. Radiographic findings: You may see calcium along the tendons in tenosynovitis.

60 posterolateral dislocation is known as a Hill Sachs fracture (well-marginated bite out of the superolateral humeral head between the greater and lesser tuberosities), resulting in a hatchet defect. The second type of humeral fracture involves a fracture of the greater tuberosity, AKA a Flap Fracture. This occurs when you avulse the greater tuberosity. Flap fractures are common with anterior humeral dislocations. The third type of fracture is a fracture through the lesser tuberosity, and this type of fracture is not common. The fourth type of fracture is a fracture through the surgical neck. This is the most common site of proximal humeral fractures. The fifth type of fracture is a fracture of the proximal shaft. If the fracture occurs proximal to the pec major attachment, the humeral head will abduct and rotate. Clinical significance: if the patient fractures the proximal shaft between the pectoralis major and deltoid, the proximal fragment will adduct. If the fracture occurs distal to the deltoid, the proximal fragment will abduct.

Fractures of the Proximal Humerus

Fractures of the proximal humerus are common with FOOSH injuries and in osteoporotic females. Minimal treatment is necessary, only to get the shoulder moving ASAP.

Fracture of the Clavicle

The clavicle can be fractured in the proximal 1/3, middle 1/3, or distal 1/3. Radiographic findings: You need tomography to see fractures of the proximal clavicle. Distal fractures can be undisplaced or displaced (the fragment goes inferiorly). Fractures through the middle part of the fractures, and the medial fragment becomes elevated and the distal fragment is displaced and angled inferiorly. Clinical significance: Proximal fractures are the least common. Distal fractures can lead to premature DJD if there has been articular involvement. Middle 1/3 fractures are prone to non-union and mal-union, exuberant callus, clavicle fractures are the most common birth trauma.

Anterior Shoulder Dislocations

There are four subtypes: subcoracoid (which is the most common), subglenoid, subclavicular, and infrathoracic dislocations. Radiographic findings: there are three associated fractures that can occur with anterior shoulder dislocations, flap fractures (avulsion of the greater tuberosity), bankart lesions (inferior labral injury) or Hill Sachs/Hatchet deformity (repeated anterior dislocations). Look for altered humeral head shape, displacement and associated soft tissue injury. The humeral head will move inferiorly and medially. Clinical significance: can also have injuries to the neurovascular bundle. Anterior dislocations are the most common.

Scapular Fracture and Bankart Lesions

The scapula can be fractured in the body (most common) or at any of the processes. A bankart lesion is an avulsion at the inferior portion of the glenoid (triceps attachments). Radiographic findings: most involve the scapular neck and the body. When the coracoid/acromion are fractured, they fracture at the narrowest part. Clinical significance: usually severe trauma is needed to fracture the scapula, via a direct blow. You can fracture your clavicle from doing push-ups!

Posterior Shoulder Dislocations

Radiographic findings: There will be a loss of elliptical overlap between the humeral head and the glenoid. Vacant glenoid sign will be present (when the glenoid is missing from the humeral head!). 6 mm rim sign (distance between the anterior rim of the glenoid to the humeral head is >6 mm, which indicates a posterior dislocation). The trough sign or reverse Hill Sachs Sign (indentation of the medial part of the humeral head) may also be present. Clinical significance: Posterior shoulder dislocations are common with seizure disorders, electrocution and falls in the elderly.

General Humeral Fractures (Flap and Hill Sachs Fractures)

There are five types of humeral fractures. The first type involves a fracture proximal to the anatomical neck, and this type of fracture is uncommon. Comminuted fractures of the humeral head are called head-splitting fractures. Impaction fractures on the

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61 Clinical significance: May occur from minor injury with mild to moderate pain. Can be post-traumatic, from RA (if bilateral), HPTH (bilateral), or scleroderma (if bilateral). Is usually visible 2-3 months after the injury, is a reaction to the injury. This is a self- limiting condition. Suggest these patients be taken off activity.

Inferior Shoulder Dislocations

These dislocations are AKA Luxatio Erecta, and are rare! They occur usually from severe hyperabduction injury. The acromion acts as a fulcrum, and fixes in hyperabduction. The patient may also present with hemarthrosis, effusion, stroke or brachial plexus neuropathy.

Elbow and Forearm Trauma

Elbow and forearm trauma usually occurs from FOOSH injuries. Radiographic findings: include fat pad signs (anterior and posteriorly). A minimum elbow series must be done (AP, lateral, oblique and tangential). Normally you might see the anterior fat pad. But the posterior fat pad is not normally seen so if you see the posterior fat pad, you know something is wrong. Clinical significance: 65% of all fractures and dislocations are at the elbow. The most common elbow fracture in the child are supracondylar fractures. The most common elbow fracture in the adult is a radial head fracture. Almost all distal humerus fractures will extend into the elbow joint.

Superior Shoulder Dislocations

Superior shoulder dislocations are rare, and a lot of force is required to superiorly dislocate the shoulder. Radiographic findings: if the glenohumeral joint measures <7 mm, suspect a rotator cuff tear. The humeral head may form a pseudoarticulation on the underside of the clavicle and the acromion. Clinical significance: Superior shoulder dislocations are often associated with rotator cuff tears.

Acromioclavicular (AC) Joint Separations

There are four grades of AC joint separations. Grade 1 AC separations are only a mild sprain. Minimal widening of the AC joint space which normally measures 0.3-0.8 cm. Coracoclavicular distance within normal range of 1.0-1.3 cm. Grade 2 AC joint separations are a moderate sprain. It involves widening of the AC joint space to 1.0-1.5 cm. Increase of 25% to 50% in coracoclavicular distance. Grade 3 AC joint separations are a severe sprain. Marked widening of the acromioclavicular joint space to 1.5 cm or more and of coracoclavicular distance by 50% of more. Dislocation in acromioclavicular joint. Apparent cephalad displacement of the distal end of clavicle. The AC view with and without weights should be taken bilaterally. Grade 4 AC joint separations occur when the clavicle is driven posteriorly. Radiographic findings: the normal AC joint space is 0.3-0.8 cm, and the normal joint space between the CC joint space is 1.0-1.3 cm.

Supracondylar Fractures of the Humerus

This is the most common fracture around the elbow in kids. Radiographic findings: The distal fragment will displace posteriorly. The anterior humeral line must always go through the middle 1/3 of the capitellum. Look for positive fat pad signs. You often dont see a fracture line with supracondylar fractures.

Intercondylar Fractures of the Humerus

Intercondylar fractures can be T or Y shaped. In 50% of adults, they can be associated with radial or ulnar fractures in a side swipe injury.

Condylar Fracture
Angular force shears of the condyle, often extending to the articular surface of the capitellum (Kochers Fracture) or trochlea.

Epicondylar Fracture
These are avulsion injuries of either your common flexor or extensor tendons. Common in baseball players who are adolescents.

Acro-Osteolysis of the Distal Clavicle

This occurs when the distal end of the clavicle is lucent with widening through the joint, and calcification in the AC joint. Radiographic findings: The distal 1-3 mm of the clavicle is affected. Usually does not progress more than 2-3 cm. May develop residual deformity with signs of healing.

Olecranon Fracture in the Proximal Ulna

Direct trauma or acute flexion with avulsion of triceps insert. 20% of adult fractures. Swelling in the bursa common.

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Coronoid Fracture
Avulsion of the brachialis, involving impaction into the trochlear fossa. These are uncommon.

Colles Fracture
A common fracture from FOOSH injuries. Radiographic findings: Posterior angulation of the distal radius, loss of normal volar tilt of the distal radius with avulsion of the ulnar styloid process is commonly associated (60%). Can be comminuted.

Radial Head Fractures and Chisel Fractures

Chisel fractures are simple vertical fractures at the articular surface of the radial head (and no further). Radiographic findings: Fat pad sign. If you see a fat pad sign in kids, a fracture will be present in 90% of cases. Clinical significance: this is the most common adult elbow injury. Chisel fractures will need to be stabilized for a short amount of time. They are easily overlooked!!

Smiths (Reversed Colles) Fracture

Occurs from a fall on hyperflexed wrist. Usually seen in elderly or kids.

Bartons (Rim) Fracture

This is a posterior rim fracture of the radial styloid, which extends through the articular margin.

Radial Neck Fractures

Most commonly, this occurs when there is impaction into the radial head. If you have a dislocation at the distal radioulnar joint, you will get a radial neck fracture. This condition is known as an Essex Lopresti Fracture. Radiographic findings: Sharp angle at the radial neck may be the only sing. Clinical significance: Can be associated with a comminuted radial head fracture.

Reverse Bartons Fracture

Fracture of the anterior rim.

Radial Styloid/Chauffeaurs Fracture (Backfire, Hutchinsons Fracture)

This is a fracture of the radial styloid with avulsion or impaction. Radiographic findings: You will see a lucency through the styloid and distal surface of the ulna.

Nightstick (Parry) Fracture

This is a transverse ulnar shaft fracture.

Monteggia Fracture
Proximal ulnar shaft fracture with an associated anterior dislocation of the proximal radius.

Fracture through the Distal Ulna/Nightstick Fracture

You will see a fracture through the ulnar styloid.

Scaphoid Fracture
This is the most common bone to fracture, and most commonly occurs in 14-40 year olds. Radiographic findings: Must do ulnar deviation view. 70% involve the waist, 20% involve the proximal pole (which is more likely to undergo AVN). Look at the fat stripe. Often occult, and if so, then treat as a fracture and re-x-ray 10-14 days later. Clinical significance: This is the most common bone to have AVN as a complication. 30% risk of non-union. The patient will present with pain in the anatomical snuff box.

Galeazzi Fracture
A radial fracture at the distal 1/3 with a dislocation of the distal radioulnar joint. Clinical significance: This is a serious condition, and can relate to compartment syndromes. The anterior interosseous nerve can be damaged.

Elbow Dislocations
The elbow can be dislocated posteriorly, posterolaterally, or distally (nursemaids elbow). Common in 2-5 year old kids. Radiographic findings: There will be no radiographic findings with nursemaids elbow. Clinical significance: In patients with nursemaids elbow, there will be decreased supination, and the radial head will slip out of the anular ligament.

Triquetrum Fracture
This is the second most common fracture in the wrist. Radiographic findings: Only seen on the lateral view.

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63

Pisiform Fracture
Radiographic findings: Can only be seen on a lateral view.

Bennetts Fracture/Skiers Fracture

A fracture through the base of the 1 metacarpal with dorsal and radial displacement. This fracture is similar to Gamekeepers fracture but this fracture is more proximal. Radiographic findings: A simple fracture through the base of the 1 metacarpal, resulting in 2 fragments.
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Lunate Dislocation
This is the most common dislocation in the hand, and results from hyperextension injury. Radiographic findings: You will see the Pie Sign. On the lateral view, the scaphoid will sit volar, the lunate should be sitting under the scaphoid.

Rolando Fracture

This is a comminuted Bennets fracture, (through the 1 metacarpal) and it is very rare.

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Scaphoid Dislocation
This is the second most common dislocation in the hand. Radiographic findings: Look for the ring or signet or Terry Thomas sign (gapping between the scaphoid and lunate). You will see an increased distance between the scaphoid and lunate on the Pa views.

Transverse Fracture through the 1st Metacarpal

This is the most common fracture in the 1 metacarpal. There are four types.
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Phalangeal Fracture
Phalangeal fractures are avulsion injury at the dorsal digital extension where it attaches to the distal phalanx. Radiographic findings: You will see a fracture at the distal shaft, intraarticular extension, an open fracture of the tufts, or baseball/mallet finger. Clinical significance: Inability to extend the DIP joint.

Perilunate Dislocation
This occurs when all bones but the lunate shift. The capitate will overlie the lunate on the PA view.

Trans-Scaphoid Perilunate Dislocation

A fracture through the waist of the scaphoid. The proximal pole will stay with the lunate, all others will shift.

Gamekeepers Thumb

Boxers Fracture

This involves a tear or complete rupture of the ulnar collateral ligament at the 1 metacarpalpahalangeal joint. Very common in skiers. Named after English gamekeepers who killed rabbits by breaking their necks between their thumb and forefinger. Clinical significance: Patient will have instability at the joint.

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A transverse fracture through the distal 2 -5 metacarpal shaft with anterior angulation. Radiographic findings: Transverse fracture through the 2 -5 metacarpal neck.
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nd

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Interphalangeal Dislocation
Etiology: hyperextension injury.

Bar-Room Fracture
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A fracture through the 5 (maybe the 4 ) metacarpal neck. Occurs when a drunken person hits something or someone.

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Mallet Finger
An avulsion of the dorsal aspect of the distal phalanx where the distal extensor tendon would attach. Clinical significance: the patient will have a difficult time extending distally.

Metacarpal Shaft Fractures

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These are most common in the 3 and 4 metacarpals. They will present with dorsal angulation.

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Metacarpal Base Fractures

These are very rare!

Arthritides
Terminology and Background Information Rheumatology is the study of disease affecting the joints, and any type of arthritic condition. Bare area = an intracapsular area of a joint (within the joint capsule) that is not protected by articular (hyaline) cartilage, leaving the bone exposed to the synovium. This region is predisposed to injury, and usually the first area that becomes eroded or inflamed. Monoarticular = only one joint is affected with the disease. Pauciarticular = 2-4 joints are affected with the disease. Polyarticular = >4 joints are affected with the disease. Osteophyte = A HORIZONTAL bony outgrowth that is continuous with the cortex and covered with a cartilaginous cap. Usually occurs where a ligament inserts near a joint. Associated with DEGENERATIVE arthritides. When describing osteophytes, always mention which joint they are located, on which side of the joint, and the soft tissue findings. (Osteophytes tend to look like a little beak sticking out from a joint). Syndesmophyte = A VERTICAL, thin inflammatory ossification within a spinal ligament or peripheral annular fiber. Ankylosing spondylitis is the gold standard. Can be marginal (delicate + symmetric) or non-marginal (bulky + discontinuous). (Look like a bridge between one vbody and the next). But the syndesmophyte does not actually connect the vbodies b/c they are located in non-osseous structures (ex: ALL). Vbodies may loose their anterior concavity and begin to look boxy/square anteriorly instead. Erosion Romulus lesion Shiny corner sign syndesmophyte. Erosion = A loss of bone due to active breakdown or pressure (ex: aortic aneurysm). Synovial fluid becomes inflamed and turns into pannus (vascularised granulation tissue), which pushes on the bone and causes it to erode. Occurs in the bare area first. Found in: Inflammatory or metabolic arthropathies. Periosteitis = AKA Periosteal Reaction. When the periosteum of the bone elevates, leading to new bone deposition. Found in: malignant tumors, infections, sometimes trauma, rarely inflammatory arthropathy. Enthesis = The transitional zone between bone and ligament/tendon. Enthesopathy = The inflammatory cellular infiltrate that gets into the bone-ligament or bone-tendon junctions and eats away at the bone, making it look like an erosion. Used when talking about inflammatory arthritides.

64 Types of Joints There are three types of joints: fibrous joints, cartilaginous joints, and synovial joints. Fibrous Joints = There is fibrous tissue (collagen) between osseous structures with no synovium. The opposing cortices are irregular. Ex: Sutures in the skull, tibia/fibula, radius/ulna interosseous membranes, and the superior 1/3 of the SI joint. Cartilaginous Joints = Fibrocartilage with some hyaline cartilage on the articular surfaces, with no synovium present. Ex: IVDs, symphysis pubis, and the sternoclavicular joint. Synovial joints = These type of joints have a membrane that secretes fluid to lubricate the joint. Hyaline cartilage covers the superior and inferior joint surface, but on the sides where the synovium meet the cortical bone directly, there is an area without hyaline coverage and protection called the bare area (see above). Patterns of Joint Involvement There are four patterns of joint involvement: uniform, non-uniform, symmetrical, or asymmetrical. Uniform = When all compartments of a joint are affected equally (i.e. the superior/medial/lateral/inferior compartments). Found in INFLAMMATORY conditions. Non-Uniform = When a certain compartment of a joint is more affected than the other compartments (i.e. the medial compartment of the knee is more affected that the lateral compartment). Found in DEGENERATIVE conditions. Symmetrical = When changes in both left and right joints appear the same (of the same joint). *You must have both left and right films to determine symmetry (i.e. The right and the left knee both show degenerative changes to the same extent). R=L. Found in INFLAMMATORY conditions. Asymmetrical = When the changes in the left and right joints are not the same (RL) (i.e. the right and left knee joints show degenerative changes, but the changes are not symmetrical, or only the left knee shows degeneration). Found in DEGENERATIVE conditions (sometimes inflammatory). FEATURE Symmetry Joints Involved Alignment Bone Density Erosions Osteophytes Periostitis Example INFLAMMATORY Symmetrical Polyarticular (>4) Abnormal Decreased Poorly defined Absent Present Rheumatoid Arthritis DEGENERATIVE Asymmetrical Monoarticular Abnormal Normal/Increased Absent Present Absent DJD METABOLIC Asymmetrical Mono/Pauciartiuclar Normal Normal Sharply defined Absent Absent Gout

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65 at the level has already exited the IVF. In the cervical spine, the most commonly affected levels are C56 > C67 > C45. Contained Paracentral Disc Herniations Contained paracentral disc herniations occur when the nucleus pulposus migrates to one side and only affects one side of the body. This is the most common type of disc herniation. Radiographic findings: An acute, abrupt bit of nuclear material protrudes paracentrally and posteriorly. Symptoms will appear on one side (the side affected). MRI is gold standard. CT uses IV/intrathecal contrast (myelopgram), so if your patient is allergic to shellfish/iodine they can go into anaphalactic shock. Clinical significance: The disc material often displaces the nerve root in the lateral recess. The nerve root below will be affected. Contained Far Lateral Disc Herniations Contained nuclear material comes out near the IVF. The disc material may affect the nerve root coming out of the IVF, not the canal. Radiographic findings: An acute, abrupt bit of nuclear material protrudes far laterally (towards the IVF). Symptoms will appear on one side (the side affected). MRI is gold standard. CT uses IV/intrathecal contrast (myelopgram), so if your patient is allergic to shellfish/iodine they can go into anaphalactic shock. Clinical significance: In far lateral disc herniations, the nuclear material can press towards the IVF, and the root of the spinal segment above can be affected as it exits the IVF, but this is RARE. So, for example, in an L4-5 disc herniation, normally in a paracentral herniation L5 is affected because L4 would have already left the IVF. But in far lateral disc herniations, L4 can be affected instead of L5 because the disc material is protruding so far laterally. Non-Contained Sequestered Discs Non-contained sequestered discs occur whtn nuclear disc material is not longer contained in the annulus fibrosis, and migrates either cephalad or caudad. AKA: Free fragment, prolapsed discs, extruded discs (M/C), sequestered discs, fragmented, floating, ruptured, amputated, wrapped or migrated discs. Clinical Significance: You do not need to take imaging for a disc herniation, as long as the patient neurology is not deteriorating, and the patient does not have any signs or symptoms of cauda equina. CT and MRI are almost the same in diagnostic accuracy in the lumbar spine, but MRI offers more levels than CT. 21% of the asymptomatic

Arthritides
There are four categories of arthritides: degenerative (M/C), inflammatory, metabolic and infectious (where you will see endplate destruction with lost disc space). Lab information is very helpful in arthritic cases, and be sure to OBSERVE your patients. Plain film radiology is best for diagnosis of arthritides.

Disc Lesions
There are five classifications of disc lesions: normal discs, bulging discs, contained central disc herniations, contained paracentral disc herniations, and non-contained sequestered discs. Normal discs have a normal concave configuration of the posterior border of the disc. Disc Bulge A bulging discs circumference has symmetric bulging of the disc, creating a convex posterior border, slightly compressing the epidural veins. Bulging discs are common in DDD (degenerative disc disease), and bulging discs are not usually clinically significant (asymptomatic). Think of it like this: imagine you have two cookies (chocolate chip, which are my favorite), then take a scoop of ice cream (lets say vanilla!) and put it in between the cookies and squish the cookies together. It might be best to actually do this (haha). The ice cream squishes out all around the entire cookie, doesnt it? This is what a bulging disc looks like! The disc material squishes out on all sides of the squished cookies! Now, eat your cookie. Radiographic findings: entire circumference of the disc is expanded. You will need an axial view on MRI to differentiate between a disc bulge and a disc herniation. Clinical significance: The disc bulge will press on the annulus fibrosus making it expand/taught. Contained Central Disc Herniations Contained central disc herniations are AKA protruded discs, herniated discs, herniated nucleus pulposis, slipped disc, and subligamentous disc herniations. They involve a focal migration of nuclear material (which is normally contained by the annulus fibrosis). Radiographic findings: An acute, abrupt bit of nuclear material protrudes centrally and posteriorly. Symptoms will appear on both sides. MRI is gold standard. CT uses IV/intrathecal contrast (myelopgram), so if your patient is allergic to shellfish/iodine they can go into anaphalactics shock. Clinical significance: Call 911 for cauda equina. Central (and paracentral) disc herniations target the nerve root of the spinal segment BELOW because the spinal nerve

 population has a disc herniation. There is 1/3 of a chance of having a surgically treatable lesion on CT/MRI in asymptomatic individuals. Just a note, remember that the spinal cord turns into the thecal sac below the L4/5 IVF. KNOW this.

66 Spotty Carpal Sign = Lucent holes in the carpals due to erosions. Squashed Carpal Sign = Carpals are surrounded by synovial joints, so they become eroded and look joined/squashed together. Terry Thomas Sign (David Letterman Sign) = When there is a huge gap between the lunate and scaphoid.

Inflammatory Arthritides Rheumatoid Factor Positive

Rheumatoid Arthritis (RA) An autoimmune, systemic and inflammatory connective tissue disorder attacking synovial joints causing inflammatory processes. Normally, RA spares the spine, however the only exception to this rule is in the cervical spine which RA loves! Funny enough, RA does not affect the paralyzed side in paralyzed people. RA usually affects people aged 20-60 YOA. Radiographic findings: Fusiform swelling, uniform loss of joint space, marginal erosions, periarticular OP, periostitis (rare), psudocysts, deformities, and ulnar deviation of MCPs. Zigzag deformity, swan neck deformities, boutonniere deformities, arthritis mutilans, spotty carpal sign, squashed carpal sign, and Terry Thomas sign. It will be bilaterally symmetrical. The radial side of the hands/bones of the hand will be affected first. Loves the distal ulna, carpals, CMC and MCP joints, and the PIPs. Never ever will RA effect the DIPs!!! The extensor carpi ulnaris tendon can be affected (BOARDS). Usually bilateral and symmetrical. You will see periarticular loss of joint space, possible subluxation, dislocation, articular and bony destruction, bony fusion and loss of joint space. The hands and feet are most commonly affected. C1/2 will undergo erosions (because it is a synovial joint). The transverse ligament can erode causing instability at C1-2. The ADI should be a maximum of 3 mm in adults and 5 mm in children. You may see pannus formation on MRI, and dens erosions. Occipital condyle/lateral mass erosions can cause basilar impression. Tapered spinous processes. Eroded and fused facet joints and disc space narrowing. RA spares the DIPS! RA Deformities in the Hand: Ulnar deviation at the MCPs (fibular deviation of phalanges) = The fingers start to deviate in the ulnar direction at the MCP joints. Zigzag deformity = when the carpals have swung in one direction, and the phalanges are swung in the opposite direction. The zig is the first swing, and the zag is the second deformity. Swan Neck Deformity = Extension of the PIP and flexion of the DIP. Boutonniere Deformity = Flexion of the PIP and extension of the DIP. The bone slips between the tendon sheaths (like a button through a button hole). Arthritis Mutilans = mutations are usually caused by resorption of bones and the consequent collapse of soft tissue.

Clinical significance: RA targets the hands and wrists (M/C), the feet, knees and hips, along with the C/S. It loves the carpals, ulnar styloid, and radiocarpal joint. Signs and symptoms include: fever, fatigue, weight loss, muscle soreness and atrophy, swelling and stiffness. Lab findings should show positive for Rheumatoid Factor (positive in 70- 95%), increased ESR (erythrocyte sedimentation rate, rises with any inflammation), increased CRP (C-reactive protein, rises with any inflammation, not specific for RA) and mild anemia. 1/3 of all patients who develop RA undergo complete and permanent remission within 2 years of onset, with or without treatment. 40% have a slow cyclic progression between acute arthritis and moderate activity. 20% will have aggressive progressive form with much debilitation and destruction. Lung pathologies are common with RA. Patients may present with low-grade fever, fatigue, weight loss, muscle soreness, and atrophy of muscles. There will be symmetrical peripheral joint pain and swelling (especially in the hands). Patients may have very limited ADLs from hand and foot problems. Juvenile Rheumatoid Arthritis/Juvenile Chronic Polyarthritis (JRA) JRA is an inflammatory arthropathy presenting in pts <16 years of age. There are two main types: RH+ and RH-. There are three subtypes: classic, polyarticular, and pauciarticular. RH+ is the less common, adult type with worse prognosis. RH- is more common, and is AKA Stills Disease. It includes muscle wasting, fever and fatigue. Classic JRA has systemic organ involvement rather than articular changes. There are no x-ray changes. Polyarticular JRA is the most common form, with the female:male ratio of 2:1. It presents bilaterally and symmetrical, and there are fewer systemic signs and symptoms. Pauciarticular or monoarticular JRA affects less than or equal to 4 joints, and likes to target females and larger joints Radiographic findings: Bird-like, thin and gracile bones with a small, receded mandible. Fine facial features. Overgrowth of epiphysis. Positive Terry Thomas Sign. Clinical Significance: Treatment is early and aggressive to try to decrease joint destruction. Medications include NSAIDS and corticosteroids to reduce inflammation, methotrexate (a chemotherapeutic), etanercept (anticytokine therapy to decrease the activity of TNF/tumor necrosis factor), inflixaimab, sulfasalazine, and hydroxychloroquine. Joint replacements may be necessary. Note: JRA can look like hemophilia (bleeding into the joints). BOTH hemophilia and RA will cause osteopenia, ballooned epiphyses, a squared off patella and a large, eroded intercondylar notch.

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Boards love this question: which tendon (and synovial sheath surrounding) causes erosion of the ulnar styloid? The Flexor Carpi Ulnaris. Protrusio Acetabuli Protrusio acetabuli can result from late stage RA. DDx for Protrusio acetabuli include: RA (if bilateral and symmetrical), inflammatory arthropathies, Pagets, Osteomalacia, old central acetabular fracture, idiopathic (mainly females), OA of hips, and Marfans. Osteolysis of the Distal Clavicle Osteolysis of the distal clavicle can result from RA or RSIs (repetivie strain injuries). The synovial joint of the shoulder becomes inflamed, leading to pannus formation (granulation tissue) which rubs on the bones to cause erosions. Radiographic findings: The distal clavicle appears eaten away, and the acromiohumeral space should be 7-11 mm. Clinical significance: If bilateral the DDx includes: RA, HPTH, Scleroderma, and Trauma. If unilateral, DDX includes Tumor, infection, trauma and RSI. Osteolysis of the distal clavicle can occur is the supraspinatus is torn.

67

Scleroderma
Scleroderma is a generalized, inflammatory connective tissue disorder affecting the skin, lungs, GI tract, heart, kidneys and MSK system. It is characterized by hardening/sclerosis of the skin and other tissues. Skin changes occur the most frequently. Radiographic findings: Acro-osteolysis of the distal phalanges and distal clavicle, atrophy of the soft tissues, and soft tissue calcifications. Clinical significance: The female: male ratio is 3:1, with onset occurring about 30-50 YOA. Skin will become tight, with atrophy of the underlying tissues and the laxity of the sift tissues is lost. Raynauds phenomenon is common. Telangioectasia (small dilated blood vessels near the surface of the skin or mucous membranes. Dysphagia (loss of peristalsis, especially in the esophagus, inability to swallow properly). Skin looks hide- bound, with loss of skin folds, rigidity, with tapering of the finger tips. Mauskopff (mouse-like facies).

Degenerative Arthritides
There are four types of degenerative arthritides: osteoarthritis, osteoarthrosis, degenerative joint disease (DJD) and degenerative disc disease (DDD). The etiology is often unknown. Primary degenerative arthritides include idiopathic origin or hereditary. Secondary causes include predisposing fators (AVN, trauma, anything causing abnormal articular function). There are three types of DJD/OA: primary, secondary or erosive. Dont worry too much about the primary or secondary types, just know that they are different from erosive. Erosive OA is an inflammatory condition. It is an exception to the rule (as opposed to DJD or OA which are non-inflammatory conditions). OA will being in a small area of a bone, and will gradually increase in size. On the radiograph, OA/DJD will appear as an asymmetric and non-uniform loss of joint space (because its non-inflammatory), and many conditions can occur as a result, including and not limited to degenerative spondylolistehsis, instability, synovial cysts, Baastrups Syndrome, hemispheric spondylosclerosis (HSS), chondromalacia patellae, Heberdens Nodes, and Bouchards Nodes. Degenerative arthritis are non-inflammatory degeneration of joint cartilage with secondary affects on the bone, and this is the most common type of arthritis we will see in practice. It is AKA osteoarthritis, so you can use the term interchangeably. Radiographic findings: Likes to target the weight-bearing joints (hips, knees, spine). In st st the hands, it loves the DIPS, PIPS and 1 metacarpal-trapezium joint. In the feet, the 1 metatarsal phalangeal joint and A/C joint is targeted. Secondary OA can target almost any joint, but it loves the DIPS! Degeneration will be asymmetrical, with non-uniform

Systemic Lupus Erythematosis (SLE)

SLE is a chronic systemic autoimmune disease that can affect any part of the body (cells, tissues undergo inflammation and tissue damage). It is fairly common, especially in young adult females. Lupus can be translated to mean wolf, and patient with SLE will have facial markings of a wolf. Radiographic findings: Bilateral and symmetrical, and loves the hands, knees, wrists and shoulders). You will see soft tissue calcifications. Clinical features: signs and symptoms include fever, malaise, anorexia and weight loss, polyarthralgia (many sore joints), skin rash, renal failure (CC), heart, lung and nervous system difficulties. The patient may present with Raynauds phenomenon, swelling, pain and stiffness. There is an increased risk of AVN. The patient will likely have a butterfly rash (across her cheese), erythematous and symmetrical, with other skin lesions on the neck, elbows, and dorsum of the hands. Lab tests which may be positive include: ANA titre (antinuclear antibodies, present in most autoimmune diseases), L.E. (lupus erythematosus cells), ANF (antinuclear factor), and abnormal plasma proteins. The patient may have normochromic, normocytic anemia, low platelets, WBCs and high ESR. DDx for bilateral and symmetrical swelling and stiffness includes SLE and RA. The hand deformities are reversible and can bend back into shape, but with RA, this is not the case.

 joint-space narrowing. Osteophytes will be seen with subchondral sclerosis (sclerosis under the joint margins because the bones are trying to heal themselves). The cartilage cracks, and the synovium will leak into the bone and create subchodnral cysts (AKA geodes) creating lucencies on the radiograph. Clinical significance: in the lumbar and cervical spine, there is a poor correlation between radiological signs and symptoms and clinical findings. Sometimes the patient will present with moderate achy pain, stiffness that is worse after rest, occasional swelling, crepitus, deformity, reduced ROM and IVF/central spinal stenosis. In OA of the knee, you wont get changes quite so bad as in other joints, you will only see subtle and osteophytic changes, and subchondral cysts wil be harder to see. The Q-angle of the knee can change, creating genu varum or valgum. Note: Valgum = think of gum sticking your knees together, valgus = knees further apart. Laboratory findings will be completely normal for these patients. Bunions st Bunions are when an osteophyte projects medially from the 1 MTP joint. This is a non- inflammatory conditions (since there are osteophytes and subchondral sclerosis). Radiographic findings: Hallux valgus of the 1 MT. The joint projects medially and the first toe projects laterally. The joint space may be decreased or maintained. Sesamoid bones can become osteophytic. Clinical significance: the etiology can be from osteoarthritis or genetics. Treatment includes conservative management or bunionectomy surgery. Spinal Stenosis The spinal canal narrows and compresses the spinal cord and nerves due to spinal degeneration associated with aging. Spinal stenosis can be caused by disc herniations, opsteoporosis, tumors, or can be congenital. Radiographic findings: If the patient has mid-saggital diameter <10 mm, this indicates absolute stenosis. If the mid-saggital diameter is between 10-12 mm, this indicates relative stenosis. The ligamentum flavum should be <5 mm thick. If its >5 mm, it can contribute to stenosis. If the AP diameter is <3 mm, this can cause lateral recess stenosis. CT is the gold standard (because its so great at assessing bone). Clinical significance: Claudication or sciatica, which is worse with standing/walking, and relieved by sitting/lying down. Note: In achondroplasia dwarfs, the interpedicular distance (distance between the pedicles) is narrowed in the first place, so a disc herniation or bulge could create stenosis easily!
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68 Lateral Recess Entrapment A condition involving a lateral recess that is not of sufficient diameter to allow the nerve root to exit freely. Narrowed at the superior border of the pedicle. Can be congenital or acquired. Can be from facet DJD or osteophytes. Most common at L45 and L5S1. Radiographic findings: Look for intermediate attenuation (grey blurry areas in the spinal canal) which could be the ligamentum flavum buckling in the canal. The normal AP measurement is 5 mm or more (<3 mm lateral recess stenosis). Pringle thought that the spinal cord looked like a puppy with floppy ears! Note: facet arthrosis contributes to IVF stenosis, centra stenosis, and lateral recess entrapment. Cervical Spondylotic Myelopathy (CSM) Pathology in the cervical spinal cord due to spondylosis (spinal stenosis which strangles the cord). Clinical significance: upper and lower limb symptoms. Symptoms can imclude weakness, numbness, and clumsiness in the upper limb. Altered walking ability, and a painful, stiff neck. Signs could include muscle wasting, loss of vibration, pinprick, pain and thermal sensation. Hyper-reflexia, clonus, L/Hermittes Phenomena, and bowel/bladder dysfunction may be present. Note: anterior osteophytes dont cause many issues, but posterior osteophytes can cause problems when they venture towards the spinal canal. OA of the Hands Radiographic findings: Osteophytes and soft tissue deviation. Clinical significance: OA of the hands prefers the DIPS (Heberdens nodes), then the PIPs (Bouchards Nodes) and then the base of thumb (in order of preference). Keep in your st head = DIPs and 1 CMC joint! You will also see osteophytes, subchondral sclerosis, and debris. There will be NO erosions. To remember that Bouchards nodes are more proximal, remember this little story from Pringle. Apparently, Bouchard was a guy who had his leg amputated, so he only had his proximal leg left. GH Joint OA Radiographic findings: OStephytes at the anterior/inferior cortex of the acromion. Note the joint space between the humeral head and acromion. Clincial significance: The GH joint doesnt like to degenerate unless there is crystal deposition, disease or trauma to the area. The supraspinatus may be affected as the osteophyte will press on its tendon.

RADIOLOGY REVIEW
AC Joint OA This joint LOVES to degenerate! Degenerative Disc Disease (DDD) This is degeneration of the IVD. Radiographic findings: Osteophytes, air (pure bloack) in the joint space (from vacuum phenomenon), subchondral sclerosis, hemispherical spondylosclerosis (sclerotic densities in the vertebral bodies), decreased disc space, and the shiny corner sign (indicates AS). The vacuum phenomenon is a process where air gets sucked in from the extracellular fluid of the surrouding tissues. It indicates a cracked or fissured annulus, the nucleus I often affected as well. This process also indicates that the pathology is not infectious. The endplates will be fine. Degenerative Spondylolisthesis This is degeneration of the discs and facets, causing one vertebra to slide forward (ex: L4 slides forward on L5). Note that in spondylolytic spondylolistheses you will see pars defects, and no pain. Degenerative spondylolistheses will be painful with degeneration. Radiographic findings: No pars defects (from DDD and remodeling of the facet joints). May get degenerative retrolistheses and lateral listheses. Clinical significance: Common in females, usually at L4. Hypermobility may cause pain, but eventually it stabilizes. This is very painful! Facet Arthrosis This is degeneration of the facet joints. Do not confuse this with a unilateral sclerotic pedicle. Dr. Pringle thinks that hypertrophied facets joints look like elf boots on axial slices! Radiographic findings: Sclerotic and hypertrophy of the facets. Clinical findings: Can cause narrowing of the lateral foramina from the hypertrophy of the facet (affecting the IVF and nerve root above). Baastrups Disease This is a condition where the spinous processes kiss (or jam into each other). Boards love this disease. Radiographic findings: Adjcanet spinous processes have come close to each other and appear to be touching.

69 Clinical significance: The etiology can be congenital and enlarged spinous processes. The condition can be painful, or pain free. Cervical Spine DDD/DJD Radiographic findings: Degeneration of the IVD, hypertrophied facets can cause IVF stenosis, hypertrophied uncovertebral joints may cause IVF stenosis, and vertebral artery compression. Sharp and point unicinate processes, blunted unicnate processes (when the uncinate processes bend over laterally). This will appear as a little lucent line within the vertebral body on the lateral view. IVFs that are hourglass shaped (from the facets and uncovertebral joints). May cause disruption of the sine wave of the AP lower cervical spine. Clinical significance: Low correlation between severity of the DJD and the cervical and lumbar spine to pain and disability. Hypermobility and instability. Foraminal or central spinal canal stenosis. Vertebral artery stenosis. Lower limb degenerative joint disease more symptomatic. Supplements: Glucosamine sulfate and chondroitin sulfate (great for DJD/DDD and EOA). Note: Posterior osteophytes can cause central canal stenosis. Uncovertebral osteophytes can cause lateral canal stenosis. When the disc spaces are narrow, then the uncinate process can get sharp, pointy uncinates and then they can tip over laterally. This can cause IVF stenosis. Also, you CANNOT get calcification in the vertebral artery! NEVER EVER. DISH (Diffuse Ideopathic Skeletal Hyperplasia) DISH is an articular disorder that loves the spine, presenting as calcification and ossification of the ALL in 3-4 contiguous segments, but you must remember that the ossification is interrupted by discal extensions. It prefers the thoracic spine, however can anywhere, but has a predilection for the axial skeleton and legamentous ossification (especially of the ALL/anterior longitudinal ligmanet). DISH tends to like the right side of the spine due to the presence of the abdominal aorta on the left. Targets the upper 1/3 of the SI joints. Patients with DISH have a predisposition to form bone, and DISH has an unknown etiology. Radiographic findings: thick flowing hyperostosis/bone formation (in the ALL and adjacent soft tissues), causing a bumpy anterior spinal contour, but the actual anterior vertebral bodies should still maintain their normal convacity (this is very important to note in your radiographic findings, since in AS, the anterior vertebral bodies will be squared-off!). Discs are relatively spared. Horizontal lucencies/clefts through the hyperostosis (due to disc preservation). Radiolucent vertical shadow between the ossified ligament and the vertebral body. Does not target the SI joints, but can affect the upper SI ligaments). OPLL (ossification of the posterior longitudinal ligament) is possibly in 50%. Intercalary bone (little bone anterior and inferior of the vertebral body, located

 in the anterior perimeter of the annulus, which starts the process of DISH). In the spine, there must be at least 4 contiguous segments affected, the disc heights must be relatively normal, and the apoplhyseal and SI joints should be normal. The hyperostosis should be 1-20 mm thick. In extraspinal sites, there will be roughened bony attachments, with ligament and tendon ossification. Clinical significance: Hyperostosis can affect the esophagus and lead to dysphagia (20% of patients). Likes to present in older patients (>40). Patients with DISH have a high correlation with Diabetes Mellitus (DM Type II) (20%). Can be associated with OPLL in 50% of cases (ossification of the posterior longitudinal ligament, see below). Usually th DISH occurs in older patients, and DISh has a male predilection, usually after the 5 decade. The patient will present with chronic, low-grade pain, with joint motion being affected. Peripheral joints may be affected. If OPLL is present, spinal stenosis may be present. Management does not require immediate referral to a rheumatologist. Note that this is not the same process as syndesmophytes. OPLL (Ossification of the Posterior Longitudinal Ligament) This condition is very commonly associated with DISH, in the Japanese and Taiwanese populations who consume a high salt and low meat diet. It is associated with obesity and glucose metabolism problems. It is the most common in the cervical spine. Clinical significance: can be symptomatic or asymptomatic. Progressive cord myelopathy causing difficulty walking. Symptoms more prominent if 60% or greater of the canal is occupied. Spinal stenosis may be present. You can treat these patients, unless they hace CSM (Cervical spondylytic myelopathy from OPLL), in which case we refer. Erosive OA Erosive OA is an inflammatory condition that may be hereditary. It usually affects women from 40-60 YOA. Erosive OA is an inflammatory condition. It is an exception to the rule (as opposed to DJD or OA which are non-inflammatory conditions). It loves the interphalangeal joints. Erosive OA will naturally follow OA, since it is an inflammatory type of DJD. Radiographic findings: Gull-wing erosions and symmetrical involvement of DIPs and PIPs st with non-uniform joint space loss. It likes the 1 CMC joint. This condition will look exactly like OA, except for the fact that there are gull-wing erosions! You will see sclerosis, osteophytes, periostitis (mouse ear sign), ankylosis, and non-uniform loss of joint space. (Boards love the gull-wing erosions)). EOA has erosions. Clinical significance: You will find warm, red and swollen joints that are aggravated by certain foods (nightshade family). Common in middle-aged females. Rheumatoid factor negative. Inflammatory markers may be positive (ESR, CRP positive), seronegative. Referral to rheumatologist. Patients will present with pain, swelling, redness and actual finger deformity.

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Seronegative Spondyloarthropaties
These are a group of diseases involving the axial skeleton, having a negative serostatus (negative for Rheumatoid Factor). It includes four conditions: ankylosing sponylitis, enteropathic spondylitis (spondylitis), reactive arthritis (Reiters Syndrome) and the undifferentiated type. Terms to know: Andersons Lesion = When a single level becomes mobile, resulting in instability and adjacent destruction that stimulates infection or neuropathy. Usually only found in advanced cases, and rare. Bamboo spine = Uniform and symmetric bridging of syndesmophytes that creates the appearance of a sine wave that should NOT be seen in the lumbar spine. Barrel Vertebra = Accentuated convexity of the anterior vertebral body. Can also be called square vertebra. Carrot Stick Fracture = A fracture through the ankylosed segment and ampifies the brittleness of the spine. If the patient comes in with sudden improvement in ROM, we worried about this. Dagger Sign: Midline vertical radioaque line on the AP lumbar film representing ossification of the supraspinous and interspinous ligament. Romanus Lesion = Erosions at the anterior vertebral body margin at the annulus insertion as a precursor to syndesmophytes formation. Rarely seen. Shiny Corner Sign = Transient reactive sclerosis adjacent to a Romanus lesion as a precursor to syndesmyphyte formation. It is not always seen. If you see osteophytes, then it is not shiny corner sign youre seeing. Star Sign = Occurs when the top of the SI joint fuses. According to Y&R, it is the ossification of the superior SI ligament creating a triangular opacity. Squared Vertebra = Loss of the normal anterior vertebral body concavity. Syndesmophyte = Inflammatory ossification of a spinal ligament. Trolley Track Sign = Three vertical lines seen on the AP lumbar film due to ossification of the facet joints, supraspinous ligament and interspinous ligaments. Leen in advanced cases. Ghost Joints = the SI joints fuse and you can barely seen the SI joint line any longer.

Radiographic findings: Tend to target the entheses (bony insertion of tendons/ligaments). All seronegative spondylarthropaties target the SI joints. All inflammatory arthritides will present with periarticular osteopenia. Clinical significance: There is usually a trigger. Also targets the gut, skin, eyes, heart, and aortic valve. They are associated with HLA-B27 in the blood (8% of the normal population have this, however). There will be increased ESR and CRP. Never ever adjust

RADIOLOGY REVIEW
an actively inflamted joint. Recommend swimming activites to maintain mobility. Refer these patients to a Rheumatologist for management (all inflammatory arthritides need rheumatologist referral). You must also promise that you will always monitor the ADI because the dens and transverse ligament of the dens can become eroded and lead to instability. Note: Seronegative means that the disease is negative for rheumatoid factor. Neat! AS (Ankylosing Spondylitis) AS is a chronic inflammatory disorder affecting articulations, ligaments, and tendons of the spine and pelvis. AS affects males and females equally, but the effects seem to be worse in males. It likes patients under the age of 40. AS is the most well-known seronegative spondyloarthropathies. There is a thought that it is the final pathway for the seronegative spondyloarthropathies. The disease starts from the SI joints, and works itself upwards through the body. It starts at the SI, then moves to the lumbosacral and thoraclombar junctions. AS occurs in synovial joints, and is a non-specific synovitis similar to RA, but is less extensive and of lower intensity. You will see fibroplasia and cartilaginous metaplasia leading to ossification. In cartilaginous joints, subchondral osteoitis is replaced by fibrous tissue that eventually ossifies. The outter annulus forms syndesmophytes. Radiographic findings: AS starts in the SI joints in young adults (HALLMARK). The SI joints will be eroded (cartilage on the iliac side is much thinner than on the sacral side, so the iliac side will be eroded first). Smooth loss of cortical bone (on the iliac side of the SI joint, in the lower 2/3). Erosions can cause a pseudo-widening of the SI joint. Sacroiliitis (erosion of the SI) eventually leads to fusion of the SI joint (known as Ghost Joint). Si joints are affected bilaterally and symmetrically (as this is an inflammatory condition). Stage 1 = Pseudowidening of the SI joint. Stage 2 = Erosions and sclerosis. Stage 3 = Ankylosis (bony fusion). The erosions may be surrounded by reactive sclerosis (shiny corner sign), usually in the thoracolumar region. Once ankylosis appears, the erosions and sclerosis disappear. Marginal syndesmophytes (vertical ossifications in the outter annulus and lateral vertebral body) present. Bamboo spine occurs when multiple contiguous segments are affected by syndesmophytes. Apophyseal joints will show erosion, sclerosis and ankylosis. The patient may be osteoporotic from diminished bone density. In the cervical spine, there may be a decreased lordosis, vertebral body and facet fusion with atlantoaxial instability, odontoid erosion, decreased vertebral body size in the lower cervical levels, with tapered spinous processes, and IVF enlargement. You may see carrot stick fractures anywhere from C5-T1. Vertebral bodies will have diminished bone density, with calcification inside the vertebral bodies. The vertebral bodies will be square. In the thoracic spine, you will see syndesmophytes, facet and costal fusion, increased kyphosis and osteoporosis. The vertebral bodies in AS will be square. In the lumbar spine, you will see decreased lordosis, sacral angle, facet fusion, trolley track sign, bamboo spine, and early involvment may show Romanus Lesions and Shiny Corner Signs. In the pelvis, you will see changes in the symphysis pubis.

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The hips will be affected bilaterally and symmetrically (inflammatory condition). There will be small osteophytes, subchondral cysts, uniform loss of joint space, and axial migration of the femoral head. The shoulders are also affected bilaterally. You will see surface erosions, hatchet erosion, and uniform loss of joint space. There may be enthesopathy at the coracoclavicular attachment at the inferior clavicular surface. In the feet, you may see enthesopathy at the calcaneous (Achilles or Plantar), and spurs (fluffy, irregular). Clinical Significance = Symptoms worse in males. The patient will present with LBP, groin or buttock pain. Pain worse in the morning with progressive stiffness (takes a long time for the stiffness to ease off). Costotransverse and costovertebral joints may fuse restricting rib excursion with breathing. AS affects younger populations, usually patients from the age of 15-35 YOA. This requires a referral to the rheumatologist. AS targets the SI joints bilaterally and then ascends up the spine. Laboratory findings will show elevated ESR, mild anemia, positive BLA-B27, and negative rheumatoid arthritis latex (seronegative). Refer to rheumatologist. Sacroillitis This was already described in AS, but to avoid confusion, heres the scoop on sacroillitis. It involves the smooth loss of cortical bone, especially along the iliac side of the SI joint. It affects the lower 2/3 of the SI joint (which is the synovial part of the SI joint). There are three stages of Sacroillitis as described above. The first stage is pseudowidening of the SI joint. The second stage is erosive and sclerotic changes. The third stage involves ankylosis of the SI joint (obliteration and eventual fusion of the SI joint). Clinical significance: If bilaterally symmetric, DDxs include: AS, ES, Reiters Syndrome, or Psoriatic Spondylitis (know these DDXs!). If bilaterally asymmetric, the DDxs include: Reiters, Psoriatic, AS and ES. These DDxs are listed from most likely to least likely. If unilateral, DDxs include: Infection, RA, Reiters Syndrome, or Psoriatic Spondylitis. Refer to Rheumatologist.

 Enteropathic Arthritis (EA) EA is a condition secondary to inflammatory bowel disease (so if you have a patient with GI problems EA should be at the top of your DDx list!). The patient may present with sacroillitis and Crohns disease or Ulcerative Colitis. Radiographic Findings: Identical to AS. Clinical significance: HLA-B27 will be positive when the SI joints are involved. Refer to rheumatologist. Note the history in these patients, as this will give it away! Radiographically, this will look like AS. But before you write AS on your exam paper, check the history is there a history of ulcerative colitis or Crohns disease? If so erase the AS and write EA, or enteropathic arthritis. Psoriatic Arthritis Psoriatic Arthritis is a condition associated with people who have psoriasis. It loves to target the hands and SI joints. Radiographic Findings: In the spine: sacroiliitis, bilaterally most commonly, and usually asymmetrically to start. Unilateral sacroillitis can occur, but is less common. Non- marginal syndesmophytes and an increased ADI. Lots of erosions. Note: Marginal syndesmophytes are delicate and symmetric. Non-marginal syndesmophytes are bulky and discontinuous. In the hands: Damage occurs in a ray pattern (involving all joints in a single digit), and is asymmetrical (unlike RA). Erosions (mouse ear erosions, which occur at the right and left lateral and distal aspect of the proximal phalange. The distal end of the proximal phalange looks like a mouse head, with the lateral aspects being the little ears. When the erosions occur at the lateral parts of the bone, the ears will disappear. Periostitis. Clinical Significance: The patient can present with changes in their finger nails (pitting), which usually indicates the DIPs are being eroded or there is osteolysis of the distal tufts. The skin of the patient will be red and flaky. Swelling of the digits is common, making the fingers look like sausages, called sausage digits. Arthritis mutilans can result when the bones become eroded, and the hands take on a different/mutilated appearance. Referral to rheumatologist. Reactive Arthritis Reactice Arthritis used to be called Reiters Syndrome. It is most often found in young men, and likes to target the lower extremity. It is usually asymmetrical. Radiographic findings: Reactive Arthritis looks identical to psoriatic arthritis, except reactive arthritis targets the lower extremity. You will see lovers heels in Reactive Arthritis (Reactive Arthritis targets the heel, causing heel pain, Achilles Tendonitis, or pain at the insertion of the patellar tendon that tries to repair itself causing a bone spur at the heel).

72 Clinical Signfiicance: There is a clinical triad associated with Reactive, and its easy to remember! Just remember this little saying: Cant see, cant pee, cant dance with me! (haha). The patient usually has conjunctivitis, urethritis, and arthritis. Reactive usually occurs secondary to an STD or GI infection such as Chlamydia trachomatis, Shigella Toxin, or Samonella). Referral to Rheumatologist.

Metabolic Arthropathies
Gout Gout is a common inflammatory condition that begins acutely. It is a condition of the rich and overindulgent caused by hyperuricemia and causing sodium monourate crystals deposited in the joints. It can also be called Padagara when it involves the big toe. Gout can be secondary to other conditions (such as hyperparathyroidism). There are four stages of gout: the first is asymptomatic (but hyperuricemic) stage, the second is the acute stage, followed by a polyarticular stage. The final stage is the chronic tophaceous stage. Radiographic findings: There may be a lab in clinical signs for up to 5-10 years, and radiographic evidence of gout is rare because the condition is well controlled by medications. The most common target site is the first MTP joint, but in general gout loves the feet and the big toe in particular. There will be soft tissue swelling and tophi (increased soft tissue density, eccentric, and not always periarticular). There will be a preservation of the joint space with marginal/periarticular/intraosseous bony erosions. Chondrocalcinosis (calcium deposition in cartilage, characteristic of gout) may also be present. The overhanging margin sign may be seen (circular uric acid crystal has pressed into the bone creating an overhanging above the area of erosions (looks like the superior overhang which is seen on the acetabulum). Spotty carpal sign. NOTE: If the joint space is not well preserved, then it may mean the joint was affected by DJD before the onset of gout. Clinical significance: Can affect post-menopausal women who are on diuretics because these patients dont secrete uric acid very well. Gout can also appear in those with a family history of gout. It targets males >40 YOA and the male:female ratio is 5:1. The patient will present with abrupt onset of a red, hot and swollen toe. Characteristic patients are on a diet high in purines (beer, steak and wine). Gout can be very painful. Sometimes gout can present with other conditions such as RA, but remember that RA is bilateral and gout is unilateral. CPPD (Calcium Pyrophosphate Dihydrate Crystal Deposition Disease) The peak onset of CPPD is 60 years of age. It presents similar to DJD in 60% of patients, but is often worse. The patients can also present with symptoms that look a lot like gout.

RADIOLOGY REVIEW
Radiographic findings: Chondrocalcinosis. CPPD loves the knees, wrists, symphysis pubis, hands, ankles, hips and elbows. Pyrophosphate arthropathy (sever OA signs in unusual target sites such as the patello-femoral joint). Capsule and synovial calcification. Possible hypertrophies of the tibial spine, joint space narrowing (typical of OA). Always look at the patello-femoral joint. Terry Thomas Sign. May affect C1-2. Note: OA does not like the patello-femoral compartment if the other compartments are normal. If the patello-femoral joint is affected and the others are normal, consider CPPD. Clinical significance: The patient will present with acute swollen joint in 20% (pseudogout), but may be asymptomatic in 20%. Laboratory findings will be normal unless joint aspiration is done (contains crystals). Typically they do not aspirate for CPPD because it will not change the plan of management. If they do aspirate the synovial fluid and it has pus in it, then there is an infection. If there are crystals present, then the condition is CPPD. CPPD can also cause problems with the transverse ligament so make sure to do a flexion radiograph if people have CPPD in the cervical spine. will give this appearance, and this is ONLY found in the atrophic form of neurotrophic arthropathy.

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Clinical Significance: Bag of Bones, painless, loss of DTRs, and swelling. Charcot foot is a condition causing weakness of the bones of the foot in people who have neutrophic arthropathy. The bones are weak enough to fracture, and can undergo shape changes with walking. Eventually, the bones collapse, and the foot becomes disfigured. Usually is due to diabetes mellitus, and the foot will literally get crunchy. It is painless so the patient has to be cautious and aware of stubbing his/her foot or stepping on things since there is no sensation. Syringomyelia Syringomyelia involves fluid filled cysts in the spinal cord (usually the cervical spine), causing a shawl-like paresthesias, and neurotrophic joints in the upper limb (atrophic form). Hypertrophic Osteoarthropathy (HOA) This is the most commonly due to bronchogenic carcinoma (up to 10% of patients will have HOA). Radiographic findings: Benign periostitis/periosteal reaction (thickening outside of the cortex of the bone. Clinical significance: There is a triad associated with HOA: digital clubbing, symptoms of arthritis, and bilateral symmetrical periostitis. DDx for benign periostitis includes: osteomyelitis (single bone, and underlying bone will look abnormal), trauma (callus), venous stasis (coon), HOA, thyroid acropachy, pachydermoperiostisis (rare). Synoviochondrometaplasia This is AKA SCMP. It is a benign arthropathy that involves loose bodies, or joint mice, and osteochondromatosis. Synovial tissues will undergo metaplasia to cartilage. SCMP can be cause by anything that leaves junk in the joint. So if you have a patient whose knee (or joint) is locking, this is usually an indication for surgical referral. It appears in 30-50 year olds, and usually in males. SCMP results when the cartilage in a joint becomes calcified or ossified, leading to joint mice. Radiographic Findings: On the radiograph, you will see loose bodies (round to ovoid, smooth, laminated or stippled, with possible trabeculation). Clinical significance: Symptoms range from nothing to pain, swelling, crepitus and locking. The knee is the most common site of involvement, but is also likes the hip, ankle, elbow and wrist.

Miscellaneous Arthropathies
Neurotrophic Arthropathy This type of arthropathy is AKA Charcot Joints. If you really want to remember this condition, GOOGLE-IT. Its a very nasty, horrible condition where the degenerative process runs wild from a loss of proprioception (and pain). The number one cause is DIABETES MELLITUS, along with syringomyelia, syphilitic tabes dorsalis (syphilis), among others. In patients with nerve problems (i.e. Diabetics), there can be a loss of proprioception and sensation in the feet. This can lead to altered joint forces and stress, which leads to a ton of joitn degeneration and instability occurring earlier than it should. Since there are no nervous reflexes (along with analgesia and ataxia), the muscles and ligaments in the foot will become very lax leading to abnormal joint mechanics, and fast degeneration fo the articular cartilage, spurs, bonfe formation, fractures and joint disorganization. Of course, the patient will not technically feel any of these changes. There are technically two types of neurotrophic arthropathy, hypertrophic and atrophic. The hypertrophic form is the classic form, where bone formation is the main feature, and is characterized by the 6 Ds (distension, density, debris, dislocation, disorganization, and destruction). The atrophic form may occur as an isolated finding, and looks like the articular ends of the bone have been surgically amputated or tapered like a licked candy cane at Christmas. Radiographic findings: Just remember the 6 Ds: Debris (SCMP), density (increase), destruction, dislocation, distension (soft tissue swelling) and disorganization. Pringle thinks that there should be 7 Ds the seventh being Disgusting. Bones can end up looking like they have been surgically amputate, or pointy like a candy-cane. No tumor

 HADD (Hydroxyapatite Deposition Disease) HADD is better known as calcific tendonitis or bursitis, and it is fairly common. It usually affects the supraspinatus tendon. Radiographic Findings: You will see cystic changes similar to subchondral cysts. The soft tissues will look very full (which could indicate tumor, trauma, infection or HADD). HADD in the longus colli: Prevertebral swelling in addition to calcific density. Self- resolving, will be over in a few weeks. Pelligrini Steida = Bleeding into the MCL secondary to trauma (myositis ossificans). Clinical Signfiicnace: The patient may have pain along the biceps region anteriorly. Ultrasound (and other conservative therapies) have been found to help paitents with HADD. If HADD occurs in the neck, the patient may have dysphagia. The soft tissues will look full (can indicate trauma, infection, tumor or HADD. NOTE: Not all tendonitis is calcific. Diseases Associated with Chondrocalcinosis Cartilage degeneration: DJD Neurotrophic Arthropathy Acromegaly

74 Erythematosus, systemic lupus Chondrocalcinosis: The Three Cs, and WHIP A DOG Or Wilsons Disease Hemochromatosis, Hemophilia, Hypothyroidism, Hyperparathyroidism (primary), Hypophosphatasia, Hypomagnesemia. Idiopathic (aging) Pseudo-gout (calcium pyrophosphate dihydrate) Amyloidosis Diabetes mellitus Ochronosis Gout Cation disease: calcium (hyperparathyroidism), copper (Wilsons disease), iron (hemochromatosis) Crystal: calcium pyrophosphate dihydrate (pseudo-gout), urate (gout). Cartilage: hydroxyapatite crystal deposition disease

Causes of Secondary OA: NOT A PHOWIE Neurogenic arthropathy Ochronosis Trauma Acromegaly, AVN Pseudogout (calcium pyrophosphate dihydrate) Hemochromatosis, Hemophilia Occupational Wilsons disease Idiopathic Erosive osteoarthritis

Cation Diseases: Ca++ Hyperparathyroidism Fe++ Hemochromatosis Cu++ Wilsons Disease

Crystal Deposition Diseases: CPPD (phosphate crystals) Gout (Sodium urate crystals) Homogentisic acid (onchronosis), causes black urine

Pnemonics for the Arthropathies

These mnemonics were mainly taken from Y&R, so enjoy! Arthritis with Demineralization: HORSE Hemophilia Osteomyelitis RA, Reiters Syndrome Scleroderma

Early OA: Early Osteo Arthritis Epiphyseal dysplasia, multiple Ochronosis Acromegaly

Neurotrophic Arthropathy: Six Ds Distension, joint (earliest finding, owing to effusion) Density (increased subchondral bone sclerosis)

RADIOLOGY REVIEW
Debris (bony intra-articular fragments) Dislocation (joint surfaces often misaligned) Disorganization (joint components usually disrupted, bag of bones) Destruction (articular bone shows loss of bone substance

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Chest Radiology
Imaging
X-Ray Standard views of the chest include the frontal chest view and the lateral chest view. Additional views include the lateral decubitus and lordotic chest view. The frontal chest view is ALWAYS do be done PA, never AP. ON the PA, the entire film will have most of the structures you want, so you wont have to collimate much. The heart is more defined and the edges will appear sharper, it will appear smaller and elongated in the PA. The lung fields will be whiter/brighter. FFD is 72 (EXAM) (low contrast) so you can see the lung markings. On the AP chest is sometimes used if the patient cannot stand up, but should NOT be used under normal circumstances. The heart is more blurry and look larger in the AP. The lung areas will appear darker, and the FFD is 40 (higher contrast) so you wont be able to see the white lung markings, but you will be able to see the vertebrae better (which doesnt help for a chest view). On the lateral chest view, the left side is always towards the film/bucky to avoid magnification of the heart. You should see the netire spine and the shoulder should be pulled out of the way. You should see the cardiac shadow (blurry area where the heart would be). The costophrenic angles should be lowest part you can see. The lateral decubitus view involve the patient lying on their side (to move the fluid/tissues out of the way) and the beam goes PA through the chest. Check for air in the pleural space. The lordotic chest view allows you to visualize the apex better. The patient can bend back or you can angle the tube cephalad to get the appropriate angulation of the ray. The lordotic view is used if you want to visualize a tumor/something in the apex of the lung. The ribs will be more angled in this view as oppsed to the AP. Breathing instructions: Ask the patient to take a deep breath in and hold it (normal breath). If the patient exhales the lungs will appear smaller, the heart will appear bigger, and the lungs will appear denser and whiter. If the person inhales too much, the heart will be taller/thinner, so you will see more ribs (you should only see 10 posteriorly) and the diaphragm will be flatter. CT Scan CT takes axial slices of the patient. The ribs will look disjointed with interruption in them (you are seeing many ribs as they angle downwards). Easy to see problems in the lungs with CT. Bone window allows you to see more bones/vasculature. The soft tissue window allows you to see the lung fields better.

Premature Osteoarthritis: COME CHAT Calcium pyrophosphate dihydrate arthropathy Ochronosis Marfans syndrome Epiphyseal dysplasia Charcot joint = neurotrophic arthropathy Hemophilic arthropathy Acromegaly Trauma

Protrusio Acetabuli: PORT: Pagets Disease Osteomalacia Rheumatoid arthritis Trauma

Spotty Carpal Bones: G S RAT Gout Sudecks atrophy Rheumatoid Arthritis Tuberculosis

Terry Thomas DDx (from Pringle): RCT RA CPPD Trauma

 Nuclear Scintigraphy Radioisitopes are taken internally and emitted radiation is captured by external detectors (gamma cameras) to form two-dimensional images. Lung-specific. Radiotracer is injected into the veins emits gamma radiation as it decays. Gamma camera scans the radiation area to create an image of the lungs. Nuclear Perfusion Scans Measures the amount of blood flow to an area. Perfusion (the passage of fluid through the lymphatic system/blood vessels to an oprgan/tissue). Perfusion is observed, recorded and quantified. Helps to find infarcts and imbolisms in the lungs. Look for areas of low uptake compared to contrast. Pulmonary Arterial Angiogram Injects contrast to look at arteries and veins. Shows the extend of the pulmonary arteries.

76 should extend centrally and it will overlap the hilum of the lungs. There are lots of lymph nodes in the hilar region, so you may see large/calcificed lymph nodes. You should be able to see the primary bronchi and arterioles. When looking at the lungs themselves, divide the lungs into 1/3s. The outter 1/3 will not have as many lung markings, the middle 1/3 will have fine and thin lung markings, and the medial 1/3 have defined lung markings. The inferior fields of the lungs have more prominent lung markings than the superior lung fields. Assess the quality of the bones in comparison to the soft tissues and the surrounding air. Just because this is a chest film and the bones are not our main focus, we are responsible for the entire film. Look at the ribs and sternum for possible fractures or lesions, note the scapula, clavicle (are there 2?), and humerus. Look at the spine. You will not see a whole lot of the vertebrae, but you should just be able to make out the disc spaces. The first rib has a lot of calcification of the costocartilage, do not hallucinate this with something else! The clavicles have a smooth radiodensity running above it called the companion shadow. This is caused by the divergent rays hitting the clavicle, and mainly caused by the platysma muscle. Calcification of the costal cartilages can actually look quite ugly, but it is common. It is continuous with the ribs (important to note), and it can go up the sternum sometimes. It can also be in the soft tissues. Do not confuse this with cancer. Look at the diaphragms from side to side. The right diaphragm should be a bit higher than the left. The cardiophrenic angle is where the heart meets the hemidiaphragm (left and right). The costophrenic angle is where the ribs meet the hemidiaphragm (left, right th and posterior). The diaphragm should be at or below the 10 rib. Look for the stomach. You should be able to see the air in the stomach, this is called Meganblasse. Remember the spelling of this word for the exam. Watch for a gastric air bubble that can indicate chronic gas syndrome called Megenblasse Syndrome. You will likely be drawn to looking at the heart. It is located in the center of the chest, 2/3 of the hart mass towards the left, and 1/3 of the heart is on the right side of the chest. The cardiothoracic ratio should be 1:2. To determine this, measure the widest part of the heart and this should be the width of the thorax itself. Examine the right atrium, left atrial appendage and left ventricle. The anterior border of the heart is formed by the right ventricle (on the lateral chest view). The posterior border is formed by the left atrium. The right border is formed by the right atrium, and the left border is formed by the left ventricle. Remember these for the exam too. The mediastium and hilam are also important to note. You will see the aortic arch or knob on the upper reading right o fthe film on the aorta. It is sometimes called the aortic knuckle. The trachea should be MIDLINE. The carina is the cartilaginous ridge within the trachea that runs anteroposteriorly between the two primary bronchi at the

Evaluating Chest X-Rays

You should see patient identification (name, DOB, ID#), and the correct date/time of the film. Assess patient positioning, technique, and inspiration. Are the right/left labels? Is it an upright or recumbent film? Was the film taken on inspiration or expiration? Is the entire thorax on the film? If the patient is too big, the entire thorax might not be on the film. In this case, you can do a spot view of the area thats missing or take the x-ray transversely if the pt is wide and short. You can used the following mnemonic to help assess quality: RIPE (rotation, inspiration, penetration and everything else). Is the patient rotated? Assess rotation by either looking at the medial clavicles or the spinous processes. Make sure that the distance between the clavicles and the sternum are equal bilaterally to assess rotation, and the spinous processes should be central. If the patient is rotated, this can simulate a pathology (i.e. simulate a mediastinal shift to the same side as the rotation, making the trachea appear deviated, and making the lung fields look like they have different densities). Did the patient over inspire, over inspire, or was the film taken mid- inspiration? If the film wasnt taken on full inspiration, the heart may appear wider than it actually is. Sometimes, patients cannot fully inspire due to pain or obesity. How is the penetration (how is the quality of the radiographic in terms of penetration and density)? We should have many shades of grey on the film. We also want a high KVP (low contrast, lots of grey). Patients are x-rayed at a very low MAS (equivalent to a 6 hour plane flight). Everything else (can you see everything? All 12 ribs, border of the cheset wall, both hemidiaphragms, and clavicles). With Chest x-rays, you want to have a search pattern, just like any other x-ray youre reading. Start from the borders of the film and work in. On the lateral view, the posterior ribs should overlap and the sternum should be seen clearly. The heart shadow

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site of the tracheal bifurcation at the lower end of the trachea. Make sure you can see the two primary bonchi, and the hila with the pulmonary arteries. Lastly, look at the lungs and pleura itself. The lungs should be more opaque inferiorly and lucent superiorly. Look at the airways, and the lung markings. Is there consolidation present or are there any interstitial markings? (See below). Look at the pleura and pleural space. You normally should not be able to see the pleura. If the pleura does become evident, then this could mean that there is fluid, calcification or fibrosis of the pleura. The costophrenic angle should be sharp, and if it is not and you see a radiographic density instead, this is called the meniscus sign and could indicate a problem with the pleura. Note: Womens breast shadow can also cause the film to look radiopaque. It is very important to pay attention to the breast shadow if there is only one breast shadow, this implies the woman had a mastectomy, and you must find out why. Perhaps the patient had breast cancer, had a mastectomy, and they you would want to check the lung for possible metastasis. On the lateral view, the hilar region sits just below the aortic arch. main bump is the left ventricle. Normally, the left ventricle should be equal to or less than the diameter of the hemidiaphragm. Look to the left costophrenic angles, which should be sharp. If the left costophrenic angle is dull, this is an indication that there is fluid in the pleural cavity.

77

Look at the right costophrenic angle. Compare the left and right lung fields by looking at the apex and intercostal spaces one at a time. You should not see pleura, but may see some at the top. White spots in the pleural space are blood vessels seen end on. The parenchyma of the lungs appear as little white lines. If you see a white line vertically at the apex of the right lung, this is known as an accessory/azygous fissure which is found in some people. Look at the soft tissues of the chest wall and breast shadows. Note how many breast shadows there are; if you see only one, perhaps this patient had a mastectomy and Metastasis are in her differential list? Do you see the diaphragm? The area below the diaphragm is the infradiaphragmatc space. The right diaphragm is often higher than the left diaphragm because the heart is on the left side. The normal difference between levels is about 1 rib interspace. Look on the reading right side of the film (patients left), do you see the big air bubble right under the diaphragm? This is known as Magenblasse. It is the air in the stomach, a gastric air bubble which normally is within 1-2 cm of the left hemidiaphragm in an upright PA. Finally, look at the bones. You should see 12 ribs on each side, and two clavicles. The clavicle is normally a bit lucent medially. Look through the mediastinum you should be able to make out the disc spaces.

Search Pattern for Upright PA

Were interested in the soft tissues here, the bones are not our first priority, otherwise wed be taking a thoracic spine x-ray. Start at the right cardiophrenic angle, and the right side of the manubrium. Look towards the right heart border (the right atrium). The right atrium should not be larger than 1/3 of the right hemidiaphragm. You will see the Right atrium (on the patients right) and the left ventricle (on the patients left) on the PA view. Look up towards the right hilar region. The right hilar region is composed of the pulmonary artery, pulmonary vein, primary bronchus and lymph nodes. The right hilus is normally less than or equal to 2.5 cm lower than the left, and its also normal to see the right hilar region more than the left because the left is superimposed over the superior vena cava. The right hilus should NEVER be higher than the left hilus (the left hilus is very difficult to see, normally).

Search Pattern for the Lateral Chest View

In the lateral chest view, both arms are helo overhead, with the left side against the fim so the heart is sharper.

Divide the radiograph into stripes and follow your search pattern that way. Look towards the ascending aorta and superior vena cava, which are often superimposed. The aorta gets covered as we get older, so its more distinguishable then. Look at the retrosternal clear space (the space behind the sternum, this should be clear). The ascending aorta is curved, but the superior vena cava is straight. Find the trachea; it should be midline. Then look to the left side of the mediastinum (Moguls). The first little bump/mogul is the aortic arch/knob, the second bump is the left hilus/pulmonary trunk/conus, and the Look at the heart. It is located very much anterior in the chest cavity. Look at the heart chambers. The 2 heart chambers that are seen on the lateral chest view are the left atrium (posteriorly) and right ventricle (anteriorly). The straight ine going into the right atrium is the inferior vena cava. The posterior heart border is made up of the left atrium.

 Look to the two hilar regions, which are superimposed. The vertebral bodies should become radiolucent as you move down the spine because the shoulder girdle is superimposed superiorly. Look at the retrocardiac clear space. Look at the posterior costophrenic angle located posteriorly and in the deepest part of the chest. Fluid accumulates here. Look at both hemidiaphragms, which can be seen posteriorly. To determine which is the right and left, know that the heart sits on the left hemidiaphragm so theres a water density (heart) on top of a water (density) diaphragm, causing a silhouette sign.

78

Thoracic Anomalies
SRBs Anomaly Partial or complete fusion of the first and second ribs, forming a solic bony plate with variable sternal articular patterns. May have partial fusion of the sternum. Lushkas Bifurcated Rib This is AKA a forked rib. The anterior end of the rib will be forked, and the fourth rib is usually affected. There is no clinical significance, but it can simulate a lung cavity. Rib Foramen This is a hole in a rib. There will be an oval shaped corticated foramen found in a posterior lower rib (most commonly). It is a congenital variant with no clinical significance. Must be differentiated from a benign bone tumor (ex: ABC or enchondroma). Rib Fusion Bony bridging over 2 ribs, can occur in both anterior and posterior ribs. Often associated with blocked vertebrae or hemivertebrae at the same level. Intrathoracic Rib A rib extending vertically down along the spine. Can come off the spine or the posterior ribs, tapering at the end. Usually found on the right side of the body. Usually insignificant, but can sometimes form fibrous attachments from the hemidiaphragm, or cause restriction in ventilation.

The Apical Lordotic View Taken AP

The tube is angled cephalad, the patient leans back and this creates a lordosis. It is taken to look at the lung apices for tumors. Clavicles are way up off the thorax so nothing is hidden.

Lobar Anatomy
The right lung has 3 lobes and 2 fissures, the oblique (major) and horizontal (minor) fissure. The left lung has only 2 lobes and one fissure (major). The lingula is the portion of the left lung that is in contact with the heart border. The inferior lobes of the lungs do not contact the heart. The middle right and lingula of the left lobe do contact the heart. If you see opaqueness lower down in the lung fields (on either the right or left), that does not contact the heart but overlaps the diaphragm, you know that the inferior lobe has been affected on that side.

Pectus Excavatum This is AKA Funnel chest. It is when the sternum is depressed (exaggerated anterior The retrosternal clear space is the area directly posterior to the sternum, and anterior to concavity of the sternum). It is the most common disorder of the chest wall. On the lateral radiograph, your findings can be confirmed because the sternum will be displaced the space. This should be clear, and free from radiopaquity. more posterior than it should, and there will be a decrease in retrosternal clear space. The retrocardial clear space is the area posterior to the heart, and it should also be clear. On the frontal x-ray, the posterior ribs will be more horizontal than on a patient without pectus excavatum, and the anterior rib will be more angled downwards. The right heart The azygos fissure is in the upper part of the right lung that the azygos vein courses border will often be obscured and displaced to lie over the spine. The right middle lobe through. The pleura can reflect around this fissure and cause the appearance of another may show increased opacity from compression. There may be splaying of the pulmonary lob called the azygos lobe. This is a normal variation and has no clinical significance. vessels. There is usually no clinical significance (EXAM).

More Anatomy
The heart is an anterior structure. The ascending aorta is anterior as well. The descending aorta and aortic knob/arch are posterior.

Pectus Carinatum This is AKA Pigeon Chest. The sternum protrudes or bows anteriorly. It is associated with Morquios Syndrome. On the lateral chest view, there will be an increased retrosternal clear space. There is usually no clinical significance.

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Costochondral Calcification Calcification within the anterior rib cartilages. Intitially can be bulbous and irregular, may demonstrate a joint-like linear lucency which simulates an upper lung or mediastinal mass. Can look traumatic, and can be easily confused with cancer.

79 Note: both atelectasis and consolidation give a silhouette sign or an abnormal silhouette sign. The Air Bronchogram Sign This occurs when the bronchi remain filled with air even if there is fluid surrounding them. The air bronchogram sign is not disease specific. Radiographic findings: The bronchi will stand out prominently due to increased contrast from changes in the surrounding lung tissue (due to pneumonic consolidation, lung collapse, or inflammatory edema in the lung tissue). DDx LIP: Lobar consolidation, Inflammatory edema, Pneumonic consolidation Atelectasis/Collapsed Lung Atelectasis is the partial (reduced volume) or complete collapse of a segment, lobe or entire lung. There will be a lack of gas exchange within the alveoli from alveolar collapse/fluid consolidatiton. Atelectasis can affect a part of or the whole lung. Alveoli will deflate. This is a sign, not a diagnosis. There are three main causes, obstruction, compression or contraction; obstruction is the most common cause. Usually, the obstruction is due to a tumor (bronchogenic carcinoma, foreign objects (peanuts or small toys, especially in kids), enlarged lymph nodes and mucous plugs, where the air distal to the obstruction gets reabsorbed and that part of the lung distal to the obstruction collapses because of collateral air drift between the lobes. Atelectasis could also be due to compression, something outside the lung compressing it (i.e. penumothorax/air in the pleural spce), check for this with rib fractures. The third reason for atelectasis is contraction, for example from pulmonaty scarring or fibrosis from old TB can cause a lung to collapse. Radiographic findings: Look for a loss of volume in the lungs and radiopaque areas (increased density). Contralateral hyerlucency. Approximation of the ribs. Movement and shifting of structures (you wont see this with pleural effusion). Structures shift towards the area(s) of collapse (hilar region, minor fissure, and trachea can shift). May see displacement of the fissures (most reliable sign, if you see this, you dont really need to look for other signs, but remember that fissures are only seen 40% of the time), elevated hemidiaphragm, crowding of vasculature, or splaying of vasculature. Normally, the horizontal fissure is horizontal and located at T4 anterior ribs around the hilum. If its displaced, its curved in the direction of the opacity. You may also see increased radiopaucity of the vertebral bodies. Indirect x-ray signs include hilar displacement (towards the density, the right hilus should never be higher than the left, and should be no lower than 2.5 cm), elevation of the diaphragm (on the same side), mediastinal shift (towards the density), narrowing of

Pulmonary Conditions and Findings

Lobar Consolidation When the alveolar spaces fill with fluid (blood, pus, water, protein or cells (tumors)). These are the types of materials that can cause consolidation, and they will all look the same on x-ray. For example, a contusion to the chest (bleeding in the lung) will look the same as pus in the lung (pneumonia) or water in the lung (heart failure/pulmonary edema). Fluid moves downward (because of gravity) so the lower lobes are affected first. Causes include pulmonary edema, infection, hemorrhage and vasculitis, chronic infiltrative disease, neoplasm, and aspiration. Radiographic findings: lungs will appear opaque, often non-uniform throughout with poorly demarcated borders/indistinct margins (look fluffy, the look sharp if they run into a chest wall or fissure). Airways may still be seen as in air bronchogram sign (which normally arent seen unless theres fluid in the lung and air still in bronchi). Consolidated areas appear dense in dependent parts of the lobe/lung. Structures shift away from the consolidation. There will be no crowding of the ribs or displacement of the minor fissure. Obliteration of vascular shadows. Silhouette sign. No signs of collapse. Consolidation is different from collapsed lung because there will be dense infiltrates, crowding of the ribs, a shift of the minor fissure, and shifting towards the density in collapse. On the lateral view, you should be able to see horizontal and oblique fissures with no displacement. If in the right upper lobe = above the minor fissure. Right middle lobe = silhouette over the heart. Right lower = silhouette over the right hemidiaphragm. Left upper = above the level of the left ventricle. Left lingula = silhouette over the left ventricle. Left lower = silhouette over the left hemidiaphragm.

DDxs The 5 Ps: Acute/baceterial pneumonia, Atypical pneumonia, Pulmonary infarction, Pulmonary TB, Pancoast tumor. Clinical Significance: There will be dullness to percussion, increased breath sounds and tactile fremitus, wheezing crackles, SOB, tachypnea and ronchi with auscultation. Consolidation usually will occur in younger people and the patient will present with a fever and the chills, a cough with sputum. It is usually caused by pneumonia (pus in the alveolar space).

 the rib cage on the side of collapse, herniation of the normal lung, and silhouette sign (only one diaphragm is seen). Clinical signficance: Incomplete lung expansion and loss of volume. Ask if a crime has been committed? DDx B MInE BABe: Bronchiogenic carcinoma, Mediastinal tumors, Interstitial fibrosis, Enlarged lymph nodes, Bronchial adenoma, Aneurysm, Bronchial TB. Pleural Effusion Excess fluid accumulates (transudate, pus or blood) in the pleura. Most common cause is congestive heart failure, but can also occur from cirrhosis with ascites, bacterial pneumonia, tuberculosis, malignancy, empyema (pus in the lung cavity), infarction, trauma or surgery. Radiographic findings: Areas of radiopacity in the pleural space and base of the lungs (gravity). Cardiomegaly (CHF). Good visualization of the minor fissure (indicates effusion because fluid accumulates in the crease causing it to increase in density). Will not see movement/shifting of the structures (atelectasis will show movement). Superolateral margin appears concave (meniscus sign). Kerly B Lines (thin linear pulmonary opacities from fluid or cellular infiltratation in the interstitium of the lungs, represent fluid back up in the interstition). Note: interstitial markings are normally more prominent medially and less prominent laterally. If the interstitial markings are more prominent laterally (or more prominent laterally than medially), this is a sign of pleural effusion. Clinical signficance: Breathing impaired by limiting lung expansion. SOB. DDx BBCE MITTS: Bacterial pneumonia, CHF (most common), cirrhosis with ascites, empyema, malignancy, infarction, trauma, TB, surgery. Pleural Calcification Calcification of the lung pleura, most commonly caused by asbestos exposure. Can also be caused by old trauma and infections/empyema, old hemothorax, old TB, silicosis of asbestosis. Radiographic findings: Calcifications appear denser than fluid, and radiopaque. Unilateral if cause is trauma or infection, bilateral is caused by asebestosis or silicosis. Clinical significance: Be sure to ask your patient about old trauma or infections. DDx: Asbestosis, Silicosis, Old TB, old hemothorax, old trauma, old infection.

80 Extrapleural Sign This is a sign that helps us to differentiate where something is located (whether in the pleural space or in the mediastinum). Causes: Rib fracture (most commonly if associated with trauma), loculated effusion, metastasis (most common if no trauma), expansile rib lesion, pleural neoplasms. Local pleural masses: pleural masses can be in the pleural space and can be well- marginated, but are most often loculated. There are four causes: loculated pleural effusion (it cant move around the fibrosis, and is not very common since most pleural fluid moves; hard to differentiate from consolidation with lateral decubitus view), metastasis to the pleura , malignant mesothelioma (big pleural mass associated with asbestos), or pleural fibroma benign mesothelioma). DDx for calcific pleural plaquing: old empyema (calcified pus in the pleural space, thes ppl smell really bad), old TB, old hemothorax/hematoma (bleed in the pleural space, like myositis ossificans traumatica but in the pleura), asbestos inhalation (pleura usually sits on top of the hemidiaphragms, very pathopneumonic), Silicosis and Talc exposure. Do not confuse calcific pleural plaquing with plaquing of the costal cartilages which is normal. DDx for unilateral/bilateral enlarged hilus = REFER OUT: Tumor (unilateral, and smoker), enlarged LN (lymphoma, TB, sarcoidosis, infection), enlarge vessels (pulmonary artery hypertension of CHF). Radiographic findings: A radiopaque convex lump extending in from the outer chest wall, AKA the Cat under the Rug sign. Angles on either side of the lump are obtuse with sharp margination. The lung smoothly tapers on either side and blends into the pleural contour. There is a sharp inner margin and indistinct outer margin. (Smooth lens shaped pleural-based density that tapers superiorly and inferiorly and its outside both the parietal and visceral layers. Note: You may lose differentiation of the rib when you have an extrapleural sign near the area (which could be a sign of lytic destruction, fracture, expansile tumors). But try not to hallucinate too much. Also, loculated pleural effusion is when pleural fluid becomes encysted between the visceral layers of the pleura and the fissures, or between partially fused visceral/parietal layers, adjacent to either the chest wall, diaphragm or mediastinum. Clinical significance: Signifies chest wall disease, either pleural disease or a mass lesion of the rib (tumor or hematoma). Plasmacytoma and ABCs are common. Meniscus Sign Radiographic findings: Sweeping concave contour in a blunted costophrenic sulcus. Look retrocardial on the lateral view!!

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Clinical significance: Pleural effusion (from transudate or exudate) or metastasis. No pneumothorax. Silhouette Sign When two areas of similar radiodensity are in anatomic contact and the interface is obliterated and becomes invisible. There is a loss of a normal border between structures, because something is in the way. You will lose the definition of the silhouette; there is no definition between black and white. We will not be able to see the margin of something because something else has come into contact with it that a similar density (two things of similar densities are overlapping). A silouette sign is an intrathoracic water density lesion in contact to the heart, aorta, or diaphragm; this identifies a pathological process. Radiographic findings: Loss of the normally well-defined sharp contour of the heart, aortic outline or diaphragm. Clinical significance: Enables you to anatomically locate a water-based lesion on what structures (or outlines of structures) you can still see. DDx: Lobar consolidation (filled with liquid instead of gas), pleural effusion (excess fluid accumulation in pleura), or atelectasis (partial collapse of lung). Plasmacytoma A malignant plasma cell tumor growing in the soft tissue/within the skeleton. The skeletal forms have other occult tumors and often occur in the posterior elements. The soft tissue forms most often occur in the upper respiratory tract. Rib Fractures Radiographic findings: Bone scans will be positive for rib fractures. Often cause the diaphragm to be elevated. Radiolucent fracture line with cortical offset (cortices dont line up). Altered rib orientation. Pleural deflection (extrapleural sign). Callus formation. Pneumothorax. Clinical significance: Uncommon in children. Rarely occur in ribs 1-3 (except with nd athletes). Weight lifters who do bench press are susceptible to fracture of their 2 rib. st Throwing athletes can often get 1 rib stress fractures. If the patient presents with flail chest (multiple/compound fractures), the patient will display paradoxical breathing (the mediastinum will shift on each breath, compressing the vasculature). The patient will likely not take a deep breath on inspiration due to the pain, and the muscle will go into spasm. Always look elsewhere (especially central) to rule out trauma (sternum, spinal). Rib fractures dont like to occur solo. Compression and burst fractures are also common.

81 Elevated Diaphragm There are three possible scenarios in the case of an elevated diaphragm. Something could be pulling the diaphragm up (atelectasis or lobar collapse), something could be below and pushing the diaphragm up (inflammation, ascites, enlarged organ or a pregnant belly), or the diaphragm itself could be problematic (splinting due to pain from trauma or phrenic nerve palsy). If unilateral, the causes can include phrenic nerve palsy, pulmonary collapse, splinting (pain), eventration (disorder when all or part of the diaphragm tissue is replaced with fibroelastic tissue causing it to weaken and compromise breathing), pleural effusion or subphrenic inflammatory disease. If the diaphragm is elevated bilaterally, the causes can include poor inspiration, obesity, ascites, pregnancy, hepatosplenomegaly, or bilateral basal lung collapse. If the diaphragm is elevated bilaterally, it is usually due to something below the diaphragm. Clinical significance: The patient will present with SOB. If exertional, this points to a cardiac issue, as opposed to a progressive SOB, in which case there are usually infiltrates present. With consolidation, tactile fremitus will increase; you may hear crackling, wheezing and bronchial sounds. Note: the phrenic nerve can be injured in surgery (you will see clips on the film) or if a mass (i.e. pancoast tumor) presses against it and impinges the nerve. Hilar Enlargement When the hilar region of the lung becomes enlarged. Radiographic fidings: Hilar shadows will be present. If the shadows are branched, then they are formed by the pulmonary vessels (vascular enlargement). Often cause by an aneurysm of the pulmonary artery. If the shadows are not branched, then they are considered to be nonvascular in nature (and usually due to lymphadenopathy). DDx: Bronchogenic carcinoma (M/C), lymphoma, infection, sarcoidosis. Mediastinal Enlargement There are no measurements to determine if the mediastinum is widened. You will have to eyeball it. To differentiate between mediastinal masses and cardiomegaly, look for areas that are extending upwards and above the level of the heart on the PA view, or anteriorly going into the retrosternal clear space. If you see masses in these spaces, the mass is likely mediastinal and not of cardiac origin.

 Anterior Mediastinal Masses Radiographic findings: You will see a shadow extending up towards the clavicle, but not to the apex of the lung). Look for a widened thyroid mass superiorly, the upper part of a mediastinum will look like a martini glass, or a widened paratracheal space. Clinical signficiance: Teratomas are usually benign, and are encapsulated. Lymphomas will have a history of fatigue or recurrent infection in the young or old. DDx TTTL: Thyroid (goiter), thymic mass, teratoma, or lymphoma. Middle Mediastinal Mass Radiographic findings: Look at the lateral view and locate the center of the mass. If the center of the the mass is in the hilar reion, its likely from the middle mediastinum. Look at the PA view first to see if the mass is actually in the mediastinum or in the lung field. If its more medial and continuous with th emediastinum, its likely not from the lung and its in the mediastinum. If the mass is lateral and you can see a clear demarcation between the mass and the mediastinum, the mass is in the lung. Clinical significance: Lymphadenopathy is a disease of the lymph nodes or swollen lymph nodes. Bronchogenic carcinoma patients will often have a history of smoking. A bronchogenic cyst is a congenital abnormality where the patient forms a cyst in the lung. Complications occur due to compression and infections. Causes LABB: Lymphadenopathy, aneurysm, bronchogenic carcinoma, or bronchogenic cyst. Posterior Mediastinal Masses Radiographic findings: If the centre of the mass looks like its closer to the vertebral column, then its most likely from the posterior mediastinum. DDx: Neurogenic tumor, Paravertebral mass, meningocele, esophageal lesion, aneurysm, or hiatal hernia. Interstitial/Infiltrative Disease These are AKA Diffuse parenchymal lung disease. This a diagnosis, not a finding. It is commonly diffuse and bilaterally. RA tends to prefer the lower lung fields, whereas AS tends to prefer the upper lung fields. Infiltrative densities are not large, they do not coalesce, and they are diffuse and bilateral. Consolidation is big, fluffy, tends to coalesce, and can be diffuse and bilateral, as opposed to infiltrative densities which are not large, do not coalesce, and are commonly diffuse and bilateral. Atelectasis is an acute problem, with x-rays needing to be taken right away, whereas infiltrative is a chronic problem, and is not linked in time with x-ray findings. A miliary pattern is used to describe TB and other disease; the densities are very tiny, diffuse and bilateral. Cystic fibrosis usually occurs in a young person who complains of

82 being SOB nearly his/her entire life. They will present with hyperinflation of the cehst because the diaphragm is low. It is normal to see a large aortic know and aortic plaquing in older patients. Patterns of infiltrative/interstitial disease: (We do not need to be able to identify these for the exam). Linear or reticular (fine, coarse) lacy looking, tiny little sharp white lines. Nodular (<1 cm) tiny dots, looks like a snow storm. Reticulonodular (combination of lacy and nodular) Honeycombing (sever fibrosis) worst one in terms of prognosis (tiny crystic spaces) Ground glass (CT only)

Reasons for differences in densities in lung fields: Mastectomy, air trapping in the lung (rare), congenital agenesis of the pectoralis muscle (rare) or rotation. Radiographical findings: Diffuse patterns, not restricted to one lobe or lung. Commonly bilateral, diffuse lacy like/nodular/both pattern. You will see linear and irregular shadows which are hallmark for interstitial diseases. The interstitial markings can be reticular (linear) or nodular (little dots). Diffuse and bilateral. May not involve the whole lung. Kerly B Lines (interstitial markings only seen in the lower part of the lung, faint horizontal lines tangential to the pleural surface of the lateral parts of the ribs. Seen with pulmonary edema and chronic heart failure). The lungs will look like a dirty windshield. Atypical pneumonia and TB will produce interstitial patterns (classic bacterial pneumonia produces consolidated lobar patterns). Asbestosis shows linear (retricular) pattern and calcific plaques may be present. May see a nodular pattern with RA that will be bilateral and diffuse. Shaggy heart sign (several tiny silhouette signs). DDx: inhaled substances (silicosis, asbestosis), drug induced (antibiotics, chemo), connective tissue diseases (RA, dermatomyositis), infection (TB, atypical pneumonia), idiopathic sarcoidosis. Diffuse Interstitial Pattern DDx: Pulmonary edema, TB, histoplasmosis, coccidiodomycosis, lymphagenic carcinoma, asbestosis, collagen, and vascular diseases. Solitary Nodules Radiographic findings: Nodules have thick hazy borders with an air/fluid level inside. Masses will appear the same, but must be >5 cm to be called a mass. Nodules are usually less than 5 cm. A cyst will be very thin and clearly defined. DDx: Bronchogenic carcinoma, hematogenous metastasis, hamartoma, infection (TB< abscess, pneumonia), hematoma, tumor (primary malignant or benign) and infarction.

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Multiple Nodules DDx: Pulmonary metastasis, lymphoma, histoplasmosis, TB, rheumatoid nodules, or Wegeners granulomatosis. Cavitating Nodules DDx: Neoplasms (primary or metastatic), infection (bacetial or granulomatous), inflammatory (rheumatoid nodule or Wegeners) or they can be congenital (bronchogenic cyst, sequestration). The most common cause of a cavitating lung nodule out of this list, are primary neoplasms. Bronchogenic Cyst Radiographic findings: Borders will be very thin and clearly defined. How to differentiate between a cavity, a cyst and a neoplasm: It depends on wall thickness. Cysts will have a wall thickness <3 mm, and cavities will have a wall thickness over 3 mm. Cysts are filled with fluid, and cavities always contain air. If the walls are over 5 mm, then the lesion is likely neoplastic. Hamartoma A hamartoma is a coin lesion that is specific to the lung, and contains calcium in it. Radiographic findings: Popcorn, stippled calcification. Clinical significance: Hamartomas are benign lesions. Note: If a tumor has stippled calcification in it, then its most likely benign. If the size of the tumor has not changed in two years, then the lesion is for sure benign. Bronchogenic Carcinoma Bronchogenic Carcinoma is the leading COD in men and women. It is the most frequently diagnosed malignancy, and can be classified into four different types: adenocarcinoma (non-smokers) (45%), squamous cell carcinoma (33%), small cell carcinoma (16%) and large cell carcinoma (6%). Bronchogenic carcinoma is a primary malignant tumor. It can cause air to get trapped in the pleural space outside of the lung, and can cause it to collapse. Bronchogenic carcinoma is a specific diagnosis causing atelectasis. Check for associated rib fractures. Radiographic findings: Atelectasis (lobar collapse because air cannot get in, mediastinal shift and tracheal deviation, narrowing of intercostal spaces, and high diaphragms). There may be segmental consolidation (masses, ex: silhouette sign), unilateral hilar enlargement, emyphsema (compensatory, because of atelectasis when the remaining lung overinflates to compensate), cavitation (hole within the cancer mass), medastinal mass, apical mass, and/or a parenchymal mass. Primary neoplasms are the most common cause of cavitating lung nodules.

83 Clinical significance: patients will usually be between 55-60 YOA. A major risk factor is smoking. The five year survival rate is 12%, and 25% are resectable at presentation. The patient will present with coughing and wheezing, night sweats, dyspnea, hemoptysis, chest pain, weight loss, clubbed fingers (due to chronic hypoxia from heart disease or lung cancer), or the patient may be completely asymptomatic (up to 50% of patients). Adenocarcinoma This is the most common type of lung cancer (45%), especially in non-smokers. Radiographic findings: Located peripherally (75% of cases), often in the upper lobes of the lung. Lesion will be lobulated or will have shaggy borders. Lesion will cavitate. Clinical significance: Most patients with adenocarcinoma will be smokers, but of the non-smokers, this is the one that will present. Adenocarcionoma metastasizes early (often to the CNS), and there is a poor prognosis with this tumor. Refer to oncologist. Squamous Cell Carcinoma This is the second most common type of lung cancer (33%) and has a strong association with smoking, but small cell has the largest. Radiographic findings: Centrally located in 66% of cases. Often presents as hilar or peripheral mass. May be radiographically occult (unable to see). Atelectasis and consolidation (50%). Most common lesion to cavitate. Clincial significance: The highest five-year survival rate because the metastasis occurs later on, therefore there is a better prognosis. May cause hypercalcemia. Refer to an oncologist. Small Cell Carcinoma Small cell carcinoma has the strongest association with smoking. Radiographic findings: centrally located (80% of the time). Both S carcinomas are centrally located. Often looks like a mediastinal lymphadenopathy. Rarely occurs as a solitary mass, and almost never cavitates. Clinical significance: Grows the fastest and has the poorest five-year survivale rate of only 3%. Small cell carcinoma frequently metastasizes, and is considered non-surgical. Refer to an oncologist. Large Cell Carcinoma This is the least common type of lung cancer (6%).

 Radiographic findings: Lesion is peripherally located (60% of cases), cavitates 5% of the time. Will present as a very large tumor, 70% of the time it will be over 4 cm. Non- cavitating. Clinical significance: Grows rapidly and metastasized early. Poor prognosis. Pancoast Tumor A pancoast tumor is an apical lung mass that can be a type of bronchogenic carcinoma (although its not one of the four main types). It is a superior sulcus tumor, and is of the non-small type carcinoma. Radiographic findings: Apical mass and bone destuction of adjacent ribs and/or spine. Metastasis can come from the lung via direct extension. Clinical singnificance: Pancoast tumors are often due to squamous cell carcinoma or adenocarcinoma. The five-year survival rate is about 10%. Patient will present with neck, arm and shoulder pain, often displaying signs and symptoms of Horners Syndrome (ptosis, miosis, anhydrosis, flushing of affected side of the face). Can cause paralysis of the phrenic nerve (causing raised phrenic nerves). Horners syndrome is a problem with the sympathetic nervous system. The patient will have miosis (pupil constriction), ptosis (drooping of the upper eye lie), enopthalmos (sunken eyes) and anhydrosis (decrease sweating) on the affected side of the face. The patient will most likely be a smoker with shoulder and neck pain with constant pain in the C7, T1 and T2 nerve distribution. The patient may exhibit atrophy of the hand muscles. Metastasis Occur via hematogenous, lymphatic or direct extension. Hematogenous spread of metastasis will cause multiple masses of varying sizes (AKA Canon Ball Mets), whereas lymphogenous spread of metastasis usually causes interstitial patterns radiating form the hila and mediastinum with a shaggy heart sign (SHIPS AND C BOATS). Usually via the pulmonary artery. Radiographic findings: usually multiple masses, smoothly rounded nodules, various sizes or uniform. Pleural effusion. Pleural mass. Usually occur at the bottom of the lung fields. Metastasis are commonly spread to the lungs from a primary (abdominal) cancer. Clinical significance: cough, hemoptysis, dyspnea or asymptomatic. Primary sites: breast, kidney, ovary and testes, colon, thyroid, sarcomas and melanomas.

84 Clinical significance: if a patient present with pericardial effusion, send them directly to the emergency. If you see an enlarged heart then send them to the ER! The exception is if the disease is an older disease that has been treated. In this case look for signs of this on the x-ray (sternal wires, mitral valve prosthesis). Cardiomegaly Mechanical instability of the heart to circulate an adequate volume of blood. With left sided failure the blood backs up in the pulmonary tissues. With right-sided failure, the blood accumulates in the venous circulation, usually secondary to left heart failure. Causes usually related to the left heart include left ventricular failure or mitral valve stenosis. There are other causes such as pulmonary fibrosis etc. Radiographic findings: Enlarged heart shadow. Redistribution of pulmonary blood flow. Interstitial edema (Thickened fissures, Kerley B lines), alveolar edema, pleural effusion. Clinical significance: Patients will present with SOB worse with activity, and a chronic non-productive cough, nocturia, pulmonary rales, pitting edema, engorged neck veins, or an enlarged liver. There will be an increased JVP. You will find these clinical findings because the fluid (blood) is backing up into the interstitium, pleura and eventually into the alveoli. Thoracic Aortic Aneurysm A localized dilation of the aorta, 50% over the normal diameter. Less common than an AAA. Clinical significance: The majority are asymptomatic. Symptoms are related to large aneurysms and include stridors, hoarseness, dysphagia or chest pain. Risk of rupture is rare if under 5 cm. If over 6 cm, there is a significant risk of rupture. If over 10%, there is a 40% risk of rupture.

Inhalation Diseases
In inhalation diseases, the interstitial spaces become more prominent, and you will see a reticular/linear pattern of interstitial markings. Pleural plaques are most commonly found in the mid zones sparing the upper and axillary region of the chest. The history is very important for differentiating between asbestosis, Lime dust exposure and Rheumatoid. If the patient has been exposed to occupational hazards for a long time, then lime dust or asbestosis exposure are more likely. If the person has achy and swollen joints (or has been diagnosed with Rheumatoid Arthritis), think Rheumatoid. Pneumoconiosis Pneumoconiosis can be either malignant or benign. If it is malignant, interstitial or infiltrative patterns will be present, and it is not malignant like cancers are malignant. In this case, malignant pneumoconiosis refers to the fact that the disease has a significant effect on the function of the lungs causing fibrosis. Malignant

Cardiovascular Conditions and Findings

Increased Cardiac Silhouette DDx: cardiomegaly (most common), pericardial effusion (fluid in the pericardial sac) or fat deposits.

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pneumoconiosis can be caused by silicosis or asbestosis. In the benign form, there will be no x-ray signs. There are many benign types, and these people will get symptoms. If you decrease exposure of the substance to the toxin (mineral or organic dusts), the x-ray will return to normal. Silicosis This is a condition caused by inhaled silicone during mining and industrial situations. Silicone is a primary compnent of the earth and therefore all miners of any sort are at risk. There will be about 20 years between first exposure and x-ray signs. Radiographic findings: Interstitial (nodular) pattern (spine pneumonic). More pronounced in upper lungs. Volume loss and fibrosis. Hilar and mediastinal LN enlargement (with or without calcification, ddx: old TB or silicosis). Clinical significance: The patient will have a history of silicosis exposure. Complications can include pulmonary fibrosis, TB, and an increased risk of lung cancer. Asbestosis From inhalation of asbestos fibers. Asbestos is usually found in mines, insulating materials, shipyards, brake linings, fibreoptics, and telecommunication cables. The patient will require >2 years exposure, with x-ray signs not evident until at least 10 years later (often 20 years). You also need more than one exposure. Family members of asbestos workers are also at risk because asbestos gets stuck in the workers clothes. Note that asbestosis exposure does not mean that the patient wil automatically get asbestosis. Deaths from asbestos are on the rise because people didnt know it was harmful for a long time. Further, smoking increases the risk of complications with asbestos exposure, increasing the risk of lung cancer 80-100 times. Radiographic findings: Diffuse interstitial/infiltrative pattern. More pronounced in lower lungs. Lungs are affected bilaterally, calcifications and plaques within the lung pleura (look dense than fluid and more radiopaque). Asbestos plaques commonly found running along the anterior ribs. Calcific pleural plaquing along the hemidiaphragms (definitive indication of asbestos exposure) Clinical significance: The patient will have a history of asbestos exposure. Can lead to fibrosis or inflammation (check with a lateral decubitus view to check for fluid movement), if theres no movement, then there are fibrotic changes). Severity depends on how long the person was exposed to and the amount inhaled. Symptoms may not be noticed for 20 years or more. The individual will be at increased risk of lung cancer, malignant mesothelioma of the pleura and peritoneum (strongly linked, not curable, rapidly fatal), and cancer of the stomach. Lime Dust Exposure A disease resulting from the inhalation of lime dust. Radiographic findings: Prominent interstitial markings bilaterally and plaques forming within the pleural spaces, indicating fibrosis.

85

Clinical significance: Can lead to fibrosis or infammation (check with a lateral decubitus view to check for fluid movement, if theres no movement, then there are fibrotic changes). Lime dust (and other occupational dusts such as coal, graphite, silica) can cause pneumoconiosis and restrictive lung disease. Most patients > 50 YOA. Smoking does not increase your risk . Rheumatoid A group of lung diseases related to rheumatoid arthritis. Radiographic findings: Bilateral fluid in the chest (pleural effusion), scarring (pulmonary fibrosis), lumps (nodules), and high blood pressure in the lungs (pulmonary hypertension). Clinical significance: Can lead to fibrosis or inflammation (check with the lateral decubitus view to check for fluid movement, if theres no movement, then there are fibrotic changes). Patients will have a history of joint pain with swollen joints, if not already diagnosed with Rheumatoid Arthritis.

Obstructive Lung Diseases

These diseases interfere with air flow entering or leaving the lung. Asthma Asthma is a chronic inflammatory disease of the airways characterized by variable/recurring symptoms, reversible airflow obstruction and bronchospasm. Radiographic findings: Chest x-ray is not that helpful in diagnosis. If the asthma is severe, you will see increased bronchial wall markings (this is the most characteristic), associated with thicker bronchial walls and inflammation, flattening of the diaphragm associated with chronic inflammation and accessory muscle use, hyperinflation, and patchy infiltrates from atelectasis. Clinical signficance: Wheezing, coughing, chest tightness, and SOB. The patient will likely be younger, with no history of smoking, symptoms worse at night or early in the morning, or with activity. Bronchiectasis Localized, irreversible dilation of part of the bronchial tree caused by destruction of the muscle and elastic tissue.

 Radiogrphic findings: Involved bronchi are dilated, inflamed and easily collapsible. Clinical signficance: airflow obstruction and impaired clearance of secretions. Purulent sputum (blue bloater). COPD Progressive disease making it difficult to breathe. There are two main forms: chronic bronchitis (long term cough and mucus), or emphysema (destruction of the lungs over time). Less air flows into and out of the airways due to a loss of elastic quality of the airways and alveoli, destruction of the walls between the alveoli, thickened and inflamed walls of the airways, or excessive mucus which clogs the airways. Most patients will have a combination of chronic bronchitis and emphysema. Causes of COPD include: chronic bronchitis, emphysema, asthma (controversy),and bronchiectasis (dilated bronchi). Radiographic findings: Most people with COPD have normal x-rays. X-rays signs may even be normal. You will see low, flat diaphragms (when the diaphragms are low, it gives the illusion that theres fluid in the lung because the lateral costophrenic angles do not look sharp). Hyperlucent lungs. Increased AP diameter of the chest wall (Barrel Chest). Tear drop shaped heart (this sign is not found in longstanding COPD, because of hypertension in pulmonary artery which causes the right ventricle to pump harder and gets bigger lifting the heart up). The lateral view will show the patients barrel chest, increased retrosternal clear space (if >2.5 cm, its ABNORMAL). Clinical significance: COPD is diagnosed through Spirometry (function tests). 50% of patients will be able to have an x-ray diagnosis. The patient will likely be a smoker, and will have difficulty breathing especially on expiration. Emphysema This is a long-term, progressive disease of the lungs that causes SOB. Destruction of the lung tissue around the alveoli makes the alveoli unable to hold their shape on exhalation. The alveoli are unable to let air out. Radiographic findings: Hyperlucent lungs, and hyperinflated lungs. Flat and depressed diaphragms. The AP diameter of the chest may be increased (barrel chest). Small peripheral vessels. Normal or enlarged pulmonary arteries. Bullae present (destructive cyst like changes in the lungs from destruction of lung parenchyma creating hyperlucencies with a thin wall around it). Walls formed by pleura, septa, or compressed lung tissue. Clinical significance: Often caused by smoking or long-term exposure to air pollution. SOB. Barrel chest. Pink puffer. Hyperresonance. Decreased tactile fremitus and breath sounds.

86 Bullous Emphysema This is a subfor of emphysema, and is not pneumothorax because with pneumothorax the normal shape of the lung is preserved and you can see a nice smooth outline of the lung. With bullous emphysema, the huge air-filled sace compress the lung. Radiographic findings: Huge air-filled sacs that compress the lung. Clinical significance: Surgery may be required to remove the air sacs. Chronic Bronchitis/Bronchiolitis Chronic inflammation of the bronchi (medium-size airways) in the lung. Clinical significance: Persistant cough with produces sputum (phlegm) and mucus for at least 3 months in 2 consecutive years.

Pneumonia
Acute/Typical Bacterial Pneumonia The most common cause of acute/typical bacterial pneumonia is Streptococcus pneumonia. It is also referred to as lobar pneumonia because it is usually confined to one lobe because bacteria are too large to travel between lobes. Radiographic findings: Inflammation and fluid build-up in a lobe. Air bronchogram sign (hyperlucent air clearly marked in the bronchioles outlines by radiopaque fluid in the alveoli). Consolidation. Infiltrates. S. aureus and S. pyogenes: ipsilateral pleural effusion and cavitation. Clinical Signficance: Productive cough. Fever, chills, pleuritic chest pain and tachypnea. Atypical Viral Pneumonia Atypical pneumonia is also known as interstitial pneumonia because it takes up space everywhere in the interstitium and surrounds the parenchyma. Viruses are very small (much smaller than bacteria) and are therefore able to travel between lobes. Atypical pneumonia is most commonly caused by Mycoplasma pneumonia. Radiogrphic findings: Atypical pneumonia is not confined to one lobe. There will be a reticular nodular pattern throughout the lungs (patchy, non-lobar infiltrate), and pleural effusion (although finding pleural effusion is uncommon with atypical pneumonia). Clinical significance: Fever, malaise, headache, non-productive cough, no physical findings. DDx: TB, mycosis, CA, infarction.

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Lung Abscess A lung abscess occurs when there is pulmonary tissue necrosis from microbial infection. The body tries to fight the infection by walling it off and forming a cavitating lesion around it. Radiographic findings: A cavitating lesion will show an air-fluid level, and have thick, shaggy borders. Pleural effusion and hilar adenopathy (enlarged lymph nodes) may be present. Clinical significance: Fever, weight loss and malaise. Four smelling purulent sputum and poor dental hygiene. DDx: TB, mycosis, cancer and infarction. Pulmonary TB (and a bit about granulomatous diseases) A bit about granulomatous diseases: TB is a granulomatous disease. Granulomas are a granular tumor or growth, usually containing lymphoid and epithelial cells, which may also contain MO (i.e. tubercular bacilli); it may involve pulomonary parenchyma, hilar regions, pleura, or mediastinum (anywhere). There are two different types of granulomatous disease: infectious and non-infectious. The infectious type of granulomatous disease is contagious, and includes TB, atypical mycobacteria, Histoplasmosis (Ohio valley, South US, St. Lawrence River), Coccioidomycosis (South US, asymptomatic), Blastomycosis, Cryptococcosis, and Actinomycosis. The non-infectious type of granulomatous disease includes the DDx of sarcoidosis. Sarcoidosis: Sacroidosis is a non-infectious gramulomatous diseases. Sarcoidosis is common in young adults, especially in SE US and Scandinavia, especially in BLACK FEMALES. Sacroidosis is often asymptomatic, with very pathologically appearing chest x- rays. In rare cases, it can be lethal. There will be interstitial disease on the x-ray, with bilaterally symmetrical hilar enlargement (classic sign, lymph node enlargement not vessels). You will also see the 1-2-3 Sign, where there are 3 areas of lymph pathology, and both hilar regions and azygous lymph nodes which is represented by enlargement of primary bronchus on the right). TB: TB is an infectious disease caused by various strains of Mycobacterium tuberculosis in humans. Most infections result in an asymptomatic latent infection that can progress to an active disease. The primary TB infection occurs via inhalation of MO which leads to pneumonia, and it can be asymptomatic. The patient may have TB and not know it, as it manifests as a cold initially if the immune system is working well, and the infection may never fully manifest itself. Reactivation is caused by initial dissemination or re-exposure. The apical and posterior segments of the UPPER LOBES will be targeted. There will be caivation, atelectasis of the upper lobes (usually, because there is less oxygen in the area), and the patient will be symptomatic during reactivation. Reactivation of TB is a

87 more serious condition. The patient will need to be on Anti-Tubercular Drugs for a long time (may be ineffective). Reactivated TB likes the apical and posterior segments. Take the apical Lordotic View if it will help. Spread through the air when people who have active TB cough, sneeze, split or inhale droplets with TB. TB is spread throughout the body via the lymphatics or the blood. Often it spreads before the immune response has started. Organisms are walled off by granulomatous reaction. Post primary or reactivated TB occurs when the TB infections is reactivated. Radiographic findings: Interstitial (nodular) pattern, Miliary TB (SPINE mnemonic). Consolidation. Cavitating mass (DDx: malignant tumor/infection). Hilar and mediastinal LN enlargement (with or without calcification, DDx: Old TB or silicosis). Calcific pleural plaquing (DDx: old TB. Hemothorax/empyema, or asbestos exposure). Coin lesion (do lateral view if usure where its located exactly). In primary TB, the upper lobe may have homogenous infiltrates. There may be segmental atelectasis, pleural effusion, ghon complexes (calcified primary focus/single calcified granuloma in the lung parenchyma), and/or Ranke complex (Ghon complex + calcified hilar lymph nodes). In post primary or reactivated TB, you will see a cavitary apical disease, amorphous calcified lymph nodes, nodules, pneumonic infiltrates, pleural effusion, a single calcified granuloma (GHON compex), RANKE complex (Ghon complex plus calcified hilar lymph nodes) and fibrosis. The infection may be confined to one apex, and may look fibrotic and consolidated at once. May see a miliary pattern (profuse, tiny, discrete, rounded pulmonic opacities <3 mm which are uniform ins size and diffusely distributed throughout the lungs, common in TB cases and sometimes in metastatic disease). Residua of past infection includes calcified lymph nodes. Clinical significance: Patients who are immunocompromised, especially those with HIV or AIDS are at greater risk of TB, those who are in the third world countries, those receiving chemotherapy and alcoholics (very common). People are usually exposed before the age of 5. The patient will have a history of past infection, a history of being unwell, or involvement of the apex of the lung. The patient may present with fatigue, weight loss, a low-grade fever, night sweats, cough (initially dry, later purulent), occasional hemopthysis, or the patient could be asymptomatic. There is a relapse rate of 5%. Refer these patients to a physician for antibiotics if active TB, and report to Canada Health or the Health Department. One of the biggest problems in patients treatment is non-compliance and improper treatment the first time around, leading to post-primary or reactivation of the TB. Old treatments include Polmbage where they insert ping pong balls into the affected lung area hoping to collapse that part of the lung so it can become anaerobic and

 macteria couldnt live there (dont try this at home). The second old treatment is thoracoplasty, which is where they cut out part of the bony thorax for the same reason as above, also creating a secondary scoliosis.

88 with pneumothorax. Make sure the pleural surface extends beyond the border of the scapula. Clinical Significance: Spontaneous pneumothorax usually presents in tall and thin patients who present with difficulty breathing and pain aggravated by too much activity. Watch these patients, as spontaneous pneumothorax can progress to tension pneumothrax. Traumatic pneumothorax is often associated with rib or spinal fractures. Hydropneumothorax occurs when fluid is present in the dependent portions of the pleural spaces. Tension pneumothorax occurs when there has been a complete collapse of the lung. Air enters the pleural space but cannot get out leading to hypotension, shock and death. Lung re-inflation is required ASAP. Patient will barely be able to breath, and will be a lot of discomfort. This is an emergency because it is life threatening; the oxygen shortage can lead to low blood pressure and progress to cardiac arrest unless treated. Pneumomediastinum is when an area of the abdomen below the hemidiaphragm becomes filled with air. You will see air below the hemidiaphragm, just superior to the liver margin. Dont confuse this with pneumothorax. Decreased breath sounds.

Pneumothorax
Pneumothorax is a collection of air/gas in the pleural cavity of the chest, between the lung and chest wall. Pneumothorax is usually seen in the emergency room and occurs when air gets trapped in the pleural space outside of the lung causing it to collapse. Pneumothorax is a specific diagnosis causing atelectasis, so check for rib fractures! It can occur spontaneously in people without chronic lung conditions (primary), or in people with underlying lung diseases (secondary pneumothorax). In primary pneumothorax, there will be no trauma or lung disease, with a rupture of bleb on the surface of the lung. Usually occurs in tall, thin and young people. In secondary pneumothorax, there is usually associated trauma or disease (trauma, rib fracture or a penetrating injury, COPD, cystic fibrosis (CF), Cancer or asthma). There are four types of pneumothorax: spontaneous, traumatic, hydropneumothorax and tension pneumothorax. Spontaneous pneumothorax is due to ruptured blebs/bullae and usually happens in tall thin men. Treatment is surgery to repair the weakened pleura. Traumatic pneumothorax occurs with trauma, so check for fractures of the ribs! Tension pneumothorax occurs as a results (secondary to) either spontaneous of traumatic pneumothorax. With every breath the patient takes, air will leave out the hold in the lung and enter the pleura, no air can escape leading to a medical emergency. Treatment includes an immediate stab wound to the chest. Radiographic findings: Visible lung edge/you will be able to see the outline of the lung which will appear as a smooth line (normally not seen). Just laterally to this line, you will see NO pleural markings. You will see water density next to the mediastinum, which is the lung that has collapsed, but the lung will have maintained its normal shape (unless theres quite a bit of scarring of the lung causing it to change shape). You will see atelectasis as well. Air will accumulate superiorly. In tension pneumothorax, the right hemidiaphragm may be inverted and lower, beginning of mediastinal shift (which indicates the start of tension pneumothorax), or whole mediastinal shift. The lung will be squeezed into a formless shadow/dense mass (causing displacement of the mediastinum) along the spine on the same side of the collapse, you will see a dense mass with lung markings close to the spine and mediastinum. The mediastinum will be displaced AWAY from the collapsed side. You will see inversion of the diaphragm (inverts and makes it go down). Fluid line does not track upwards and laterally because negative pressure has been lost (vs. pelural effusion where fluid level tracks upward and laterally creating a meniscus sign). You will see a very large and black lung. Look at the shape of the mediastinum and the edge of the side of the blackness. If it is concave to the side of the blackness, suspect tension pneumothorax. Make sure to define the border of the scapula, and dont mix this up

Nodules
Calcified Granuloma A granuloma is a spherical mass of chronic immune cells that forms when the immune system attempts to wall off substances perceived as foreign (but unable to eliminate, such as bacteria and fungi, keratin and suture fragments). A calcified granuloma is a granuloma with calcium deposits inside it. Assume that a calcified granuloma is an old granuloma (and therefore, is benign). Note: The acute phase of histoplasmosis is characterized by non-specific respiratory symptoms, often cough or flu-like. Chest x-ray findings will be normal in 40-70% of patients. Chronic histoplasmosis cases can resemble tuberculosis. Lesions tend to calcify as they heal. Causes: histoplasmosis (most commonly, a fungal infection), tuberculosis, or malignancy (rare). Multiple Pulmonary Nodules This is when there are tons of nodules in the lung field. Must be under 5 cm to be considered a nodule. If the lesions are over 5 cm, they are considered masses. Multiple pulmonary nodules are the most common form of metastatic solid organ malignancy when over 1 cm in diameter, and are more likely benign when they are <5 mm and the patient doesnt have a history of malignant tumors. Causes: pulmonary metastasis (most commonly), lymphoma, histoplasmosis, TB, rheumatoid nodules, Wegeners Granulomatosis.

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Pulmonary Metastasis Pulmonary metastasis occur when fragements of the primary tumor become dislodged after venous invasion and are carried as tumor emboli to the lung via systemic circulation. Can also be pread via the blood or by direct extension. Usually, metastasis are spread via the pulmonary artery. Most of these fragments will lodge in small pulmonary arteries/arterioles where they proliferate and extend into the lung parenchyma and form nodules. These nodules are usually located subpleurally or in the bases of the lungs. Radiographic findings: Look at the bone structures for signs of destruction or a blastic response. Usually multiple masses. Smoothly rounded nodules. Various sizes or uniform. Pleural effusion and a pleural mass. Clinical significance: Ask about the signs/symptoms of cancer. Cough, hemptysis, dyspnea, or asymptomatic. Can commonly spread from the breast, kidney, ovary/testes, colon, thyroid, sarcomas and melanoma. Lymphoma Radiographic findings: Diffuse and nodular appearing nodules in the lungs. Note: Diffuse = lymphaomatous cells spread out, nodular = clustered together. Clinical significance: Younger patient presenting with swollen lymph nodes with signs and symptoms of cancer. Histoplasmosis An infection due to histoplasma capsulatum fungus affecting the lungs (mainly). The fungus is inhaled into the alveolar spaces where it germinates and transforms into budding yeast cells. It is not contagious, but is contracted by inhalation of spres from the soil/guano. Clinical significance: If the patient loves to garden, think of histoplasmosis. Tuberculosis Contagious bacterial infection that involves the lungs, and can spread to other organs. It is caused by Mycobacterium tuberculosis. You can get TB from inhaling air droplets from a cough/sneeze of someone who has TB. Radiogrphic findings: Lesions are often seen in the upper lungs with or without mediastinal or hilar lymphadenopathy, however lesions may appear anywhere in the lungs. You may see infiltrate or consolidation, or a cavitating lesion. Nodule with poorly defined margins, pleural effusion, hilar or mediastinal lymphadenopathy, or linear interstitial disease. Rheumatoid Nodules Usually occur in chronic active cases of RA. They are commonly associated with joint deformity and serious extra-artciular manifestations in the lungs, eyes, and blood vessels. Nodules will vary in size. See above for the skeletal symptoms of RA, and for the effects of Rheumatoid on the lungs. Wegeners Granulomatosis This is a rare disorder of vasculitis. The blood vessels will become inflamed (making it hard for blood to flow). The cause is unknown, but it is though to be an autoimmune disorder. Radiographic findings: Pulmonary nodules (coin lesions), infiltrates, cavitary lesions, pulmonary hemorrhage (causing hemoptysis), and consolidation. Clinical significance: Suspect Wegeners Granulomatosis only when a patient has unexplained symptoms for a long period of time (history of being unwell). Rhinitis is usually the first sign in patients.

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Cardiovascular Imaging
You will see increased cardiac silhouettes, and causes include: cardiomegaly, pericardial effusion or fat deposits. Cardiomegaly is the most common cause. It is usually related to left sided problems. Determine if the heart is big and if the lungs look normal. In pericardial effusion, the heart will look larger from the fluid in the pericardial sac. The heart will look large, rounded and globular (like a floppy water balloon). The heart will take on a water bottle configuration, and will have a symmetrically enlarged cardiac silhouette. Lastly, increased cardiac silhouette can be caused by increased fat deposit around the heart. Pericarditis This causes a huge heart. The left ventricle shouldnt extend > the hemidiaphragm, and the right ventricle shouldnt extend > 1/3 of the hemidiaphragm. Can be due to cardiomegaly (whole heart enlarged) or enlargement of certain chambers. Enlargement of the left ventricle leads to systemic hypertension. On the PA view you will see a bulge of the lower heart border that goes down and out. Often seen in systemic hypertension. Example given of LV enlargement due to ventricular aneurysm secondary to a previous MI. Enlargement of the left atria is usually due to mitral valve stenosis (usually due to strep throat and RHF). On the PA view, you will see a double density representing the LA aand RA. You will see an extra mogul on the lateral view representing posterior enlargement. Often due to mitral valve stenosis (most commonly by strep throat and RHF).

 RV enlargement is usually due to interstitial disease/PAH. On the PA view, you will see elevation of the cardiac apex. On the lateral view you will see obliteration of the anterior clear space. RV enlargement is often due to interstitial/infiltrative lung disease (because the right heart has to pump harder) and PAH (Pulmonary artery hypertension). RA enlargement is not as important for us. On the PA view you will see a prominent superior heart border. This is hard to differentiate from RV enlargement and the two usually go together. Radiographic findings: Cardiac enlargement. This is not a reliable sign on x-ray, and can only guesstimate. In order to do that, they need a full inspiration film with a FFD of 72 inches (same as lateral cervical). ECG is better to determine which chamber is enlarged. Congestive Heart Failure (CHF) Heart failure is the most common cause of pulmonary edema, but kidney disease can do it because of electrolyte imbalances. This is the mechanical inability of the heart to circulate an adequate volume of blood throughout the body, causing redistribution of pulmonary blood flow. With left sided heart failure, the blood backs up into the pulmonary tissues. With right sided heart failure, the fluid accumulates in the venous circulation. Right sided heart failure is secondary to left sided heart failure. Note: CHF is the most common cause of pleural effusion! Radiographic findings: You will often see prominence of vessels towards the apices or superior aspects of the lungs since the blood is backing up in that direction/intravascular congestion (Viking Helmet Sign = dilation or prominence of upper lobe vessels). You will see an enlarged heart shadow (huge heart, LV enlargement), redistribution of pulmonary blood flow, interstitial edema (fluid pressure in the vessels increases and causes leakage into the interstitium, thickened fissures and Kerley B Lines), and alveolar edema (bat wing/butterfly wing configuration, which is bilateral perihilar shadowing from alveolar edema, sparing the outer 1/3 of the lung). You will see pleural effusion (from increased pressure in the blood vessels so the fluid has no where to go but the pleural space), and usually the lower lobes of the lungs are affected more than the upper. Note: Cephalization of blood flow is when the fluid backs up into the superior vessels of the lung fields. Also, the best place for fluid to back up into is the interstitium and the fissures, which is why you will see a very prominent median fissure and Kerley B lines (since fluid is radiopaque). Blurring of the perihilar regions from fluid building up and radiating out from the hilar region. Clinical Significance: SOB worse with activity. The patient will present with a chronic, non-productive cough, nocturia, pulmonary rales (crackles), pitting edema, engorged neck veins, an enlarged liver, increased JVP, exertional SOB, ascites, pitting edema and cyanosis. Progressive dyspnea which is worse when they lay down.

90 Lasix: This causes the patient to pee out a lot of the excess fluid but along with the fluid, they also lose electrolytes. Therefore, these patients will be low in K which presents as musculskeletal complaints. You can do all the chiro treatment you want, but until they increase their K, these patients will always have musculoskeletal pain. Feed them bananas and oranges to increase their K. Digitalis: Given to increase the force of heart contractions. Thoracic Aortic Aneurysm An aneurysm is an abnormal widening or ballooning of an artery from weakness in the wall of the vessel. A localized dilation of the aorta (over 50% its normal diameter). AAA are most common (abdominal aortic aneurysm). Thoracic Aortic Aneurysms (TAA) are very common in the abdominal aorta, but not as common in the thoracic aorta. If can be very difficult to differentiate between an aneurysm of the thoracic arota and the normal changes of the aorta with aging. Normally, over time, the aorta loses elasticity and uncoils, appearing as though it is enlarged. Causes of TAAs include: atherosclerosis, syphilis, trauma (screen for thoracic aortic aneurysm when you find a sternal fracture), infection, and Marfans (Check for TAAs!). Radiographic findings: If the thoracic aorta is >6-8 cm across, this is a BIG RED FLAG for an aneurysm! Clinical significance: Risk of rupture is rare if the aneurysm is <5 cm. Risk increases significantly if they are >6 cm. 40% of aneurysms rupture if they are over 10 cm. Tramatic rupture can occur. Most are asymptomatic, or the patient can present with a stridor, hoarseness, dysphagia, and chest pain. Pulmonary Hypertension Pulmonary hypertension occurs secondary to lung fibrosis. There are two types: arterial pulmonary hypertension and venous pulmonary hypertension. Arterial pulmonary hypertension presents with bilateral hilar enlargement due to vessels, and is precapillary (PAH). Venous pulmonary hypertension is CHF, and post-capillary (LVF).

Hernias
There are four differential diagnoses for diaphragmatic hernias: Hiatal hernias, Morgagni hernias, Bochkalek Hernias and Traumatic Hernias. Hiatal hernias can be see in older females. You will see an air-fluid behind the heart in the retrocardiac clear space, superimposed over the heart in upright PA. Patient will often complain of heartburn, worse when lying down and especially after a large meal. Morgagni hernias occur anterior behind the sternum. Bochdalek hernias occur posterior on either side of the film. Traumatic hernias occur usually on the left side, when the left side ruptures because the liver tends to protect the right hemidiaphragm.

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91 Sign Lobar Consolidation Acronym: 5 Ps Differentials Acute bacterial Pneumonia Atypical Pneumonia Pulmonary tuberculosis Pulmonary infarction Pancoast tumor Lung collapse Inflammatory edema in the lung tissue Pneumonic consolidation Aneurysm Bronchogenic carcinoma Bronchial adenoma Bronchial tuberculosis Enlarged lymph nodes Interstitial fibrosis Mediastinal tumor Congestive heart failure (M/C)* Cirrhosis with ascites Bacterial pneumonia Tuberculosis Malignancy Empyema Infarction Trauma Surgery Asbestos exposure (M/C) Old trauma Old infection/empyema Old hemothorax Old TB Silicosis Rib fracture (M/C) Loculated effusion Metastasis Expansile rib lesion Pleural neoplasms Pleural effusion (transudative or exudative) Metastasis Lobar consolidation Pleural effusion Atelectasis

Review Comparisons
Collapse vs. Consolidation In collapse/atelectasis situations, structures move TOWARDS the collapse (ex. The medial fissure). Collapse causes a vacuum type effect and pulls things towards it. You will also see dense infiltrates and crowding of ribs. In consolidation, structures will shift away from the density, causing an undisplaced minor fissure, with no crowding of the ribs. Consolidation takes up space, and pushes things away from it. Pneumothorax vs. Tension Pneumothorax In pneumothorax, there will be a collection of air/gas in the pleural cavity of the best between the lung and chest wall. It can occur spontaneously with chronic lung conditions (primary) or in those with lung disease (secondary) and many pneumothraces occur after trauma. In Tension Pneumothorax, you will see medastinal shifting. Interstitial Pattern vs. Consolidation In interstitial patterns, the interstitial spaces between the alveoli of the lungs can be seen. Something is occurring in the interstitium of the lung, making the interstitial markings more visible. In consolidation, you will see solidification into a firm, dense mass. The region of tissue in the lung will become fluid-filled. Diaphragm Elevation vs. Pleural Effusion An elevated diaphragm is caused by something underneath the diaphragm pushing it up, something above it pulling it up, or a pathology of the diaphragm (or phrenic nerve) itself. The costophrenic angle will be maintained. In pleural effusion, the costophrenic angle will be obliterated causing a meniscus sign.

Air Bronchogram Acronym: LIP: Atelectasis

Pleural Effusion

Pleural Calcification

Extrapleural Sign

Chest Differentials
Sign Radiopaque Lung Differentials Pleural effusion, plaques or masses Lobar collapse, pneumonectomy Pulmonary masses or fibrosis Consolidation Meniscus Sign

Silhouette Sign

 Sign Elevated Diaphragm Differentials Pulling the diaphragm up: atelectasis. Pushing the diaphragm up: inflammation, ascites, enlarged organ or pregnant belly. Pathology of the diaphragm: splinting, phrenic nerve palsy. Unilateral: phrenic nerve palsy, pulmonary collapse, splinting, eventration, pleural effusion or subphrenic inflammatory disease. Bilateral: poor inspiration, obesity, ascites, pregnancy, hepatosplenomegaly, bilateral basal lung collapse. Bronchogenic carcinoma (M/C) Lymphoma Infection Sarcoidosis Thyroid (goiter) Thymic Mass Teratoma Lymphoma Lymphadenopathy Bronchogenic carcinoma Aneurysm Bronchogenic cyst Neurogenic tumor Paravertebral mass Meningocele Esophageal lesion Aneurysm Hiatus Hernia Inhaled substances (silicosis, asbestosis) Drug induced (antibiotics, chemo) Connective Tissue Disease (RA, Dermatomyositis) Infection (TB, atypical pneumonia) Idiopathic Sarcoidosis

Sign Diffuse Interstitial Pattern

Solitary Nodule

Hilar Enlargement

Multiple Pulmonary Nodules

Anterior Mediastinal Masses (Acronym: TTTL)

Cavitating Nodules

Middle Mediastinal Mass

Posterior Mediastinal Masses

Increased cardiac silhouette:

Interstitial Diseases

Cardiomegaly

Local Pleural Masses (could be in the pleural space and well marginated, but are most often loculated)

92 Differentials Pulmonary edema TB Histoplasmosis Coccidiodmycosis Lymphagenic carcinoma Abestosis Collagen Diseases Vascular diseases Benign tumor (hamartoma) Malignant tumor (bronchogenic carcinoma or metastasis) Infection (pneumonia, abscess, TB) Infarction Rheumatoid Nodule Pulmonary metastasis Lymphoma Histoplasmosis TB Rheumatoid nodules Wegeners granulomatosis Neoplasm (Primary or metastasis) Infection (bacterial, granulomatous (TB), pneumonia) Inflammatory (Rheumatoid nodule or Wegeners) Congenital (bronchogenic cyst, sequestration) Abscess Infarction Cardiomegaly (M/C) Pericardial effusion Fat Deposit Left heart failure (left ventricular failure or mitral stenosis) Pulmonary fibrosis Locaulated pleural fluid Metastasis to the pleura Malignant Mesothelioma Pleural fibroma

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Sign SHIPS AND C BOATS (DDx list for Interstitial lung disease) From Pringle (not in text books) Differentials Sarcoidosis (or other granulomatous disease) Histiocytosis (Eosinophilic granuloma silver dollar sign) Infection (TB etc) Pneumoconioses (silicosis and asbestosis) Scleroderma (tight skin, difficulty swallowing) Amyloidosis (deposition of amyloid interstitially secondary to RA/MM) Neoplasm (metastatic dissemination, Lymphoma, lymphatic mets) Drug sensitivity/allergy Cystic FIbrosis Bronchiectasis (dilation of bronchi) Oil Aspiration (mineral oil usually used to be in laxatives)/ Pulmonary edema Arthritis (RA, AS, usually long standing arthritis) Tuberous Sclerosis (rare familial condition like Neurofibromatosis but clinically different; other effects include mental retardation, seizures, skin lesions, bone lesions) Sarcoidosis Pneumoconiosis Infection Neoplasm Eosinophilic Granuloma Pulmonary edema Infection Hemorrhage and Vasculitis Chronic infiltrative disease Neoplasm Aspiration Tumor (unilateral, and smoker) Enlarged LN (lymphoma, TB, sarcoidosis, infection) Enlarge vessels (pulmonary artery Pleural fluid

93 hypertension of CHF). CHF (causes pelural fluid more on R) Neoplasm (Malignant mesothelioma) Infection Trauma (blood, pus, cells, water) Collagen Diseases (SLE) Pulmonary Embolus Obstruction of Great Veins (TB) Infradiaphragmatic causes (pancreatitis, ascites can penetrate the diaphragm) Hiatal Morgagni Bochdalek Traumatic Granuloma Primary Lung Cancer (Bronchog.) Mets to lung (solitary focus) Mehartoma (benign tumor) Mescellaneous: Pneumoina, AV fistula, chest wall lesion.

Diaphragmatic Hernias DDx (We didnt go over in class)

Coin Lesion DDx

SPINE for Interstitial Nodular Disease

Causes of Consolidation

Unilateral/bilateral enlarged hilus (REFER OUT)

Radiology Promises
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. I promise to do a complete search pattern on every view. I promise to take a complete diagnostic series. I promise to take separate AP lower cervical and AP open mouth views. I promise to do a flexion lateral upper cervical view before adjusting patients with RA (or other inflammatory arthropathies). I promise to do a flexion lateral upper cervical view before adjusting patients with Downs syndrome. th I promise to include the base of the 5 metatarsal on my ankle views. I promise to include the ulnar deviation wrist view on all trauma wrist patients. I promise to NEVER USE THE TUNING FORK as a substitute for x-ray in the diagnosis of a fracture. I promise not to confuse uncovertebral joint degeneration with a fracture on the lateral cervical view. I promise not to confuse normal facet joints with pars defects on lateral lumbar views. I promise to never call a limbus bone a new tear drop or compression fracture. I promise to never call the normal posterior wedging of the body of L5 a compression fracture. I promise to open the collimation on lateral lumbar views in older patients to assess the aorta. I promise never to hallucinate fusion of the C2-3 facet joints on the lateral cervical view unless there are other signs of congenital block at that level or inflammatory arthropathy in the cervical spine. I promise to NEVER hallucinate calcification of the vertebral arteries EVER!!!! I promise not to confuse the normal deltoid tuberosity of the humerus with a bone tumour. I promise not to confuse the normal cystic appearance of the greater tuberosity viewed end-on on the internal rotation shoulder view with a bone tumour or cyst. I promise not to tell my patients that the osteophytes on the anterior body margins of the lumbar vertebrae may poke into their abdominal aorta. I promise not to tell my patients that the pars defects discovered in adulthood are the result of a recent traumatic event. I promise not to confuse secondary ossification centres with fractures. I promise to check for Diabetes and OPLL in patients with DISH.

94 22. I promise not to call normal bifid spinous processes of the cervical spine spina bifida. 23. I promise to do a urinalysis on patients who have lumbar TVP fractures. 24. In patients with L5 TVP fractures, I promise to evaluate the SI joints and pelvis for diastasis and fractures. 25. I promise to never call mastoid air cells a bubbly lytic tumour. 26. I promise never to take flexion/extension lateral cervical views on a patient who has had very recent neck trauma without first evaluating the neutral views. 27. I promise to remember that the L5-S1 IVFs appear smaller normally on the lateral view. 28. I promise to not call the rhomboid fossa of the clavicle a lytic lesion. 29. I promise to use the bright light on all dark areas of the film. From Dr. B. Hsu 1. 2. 3. 4. 5. 6. 7. 8. 9. I promise not to mistake degenerated uncovertebral joints causing foraminal encroachment as posterior osteophytes. I promise not to confuse the slightly rotated superior facet of S1 as osseous encroachment of the L5-S1 foramen. I promise to identify the L5 vertebra by using the iliac crest level on frontal and lateral views. I promise not to call the normal size TVP of L5 as spatulated. I promise to look at the name plate on the film to make sure it belongs to the patient I am treating. I promise not to submit outdated films that may not have any clinical relevance to the patients current complaint. I promise to submit those films that are relevant to the region of the patients current complaint. I promise to submit films with relevant clinical information i.e. duration and location of complaint, history of trauma, malignancy or surgery. I promise not to mistake the posterior border of the acromion as the landmark for assessing the acromiohumeral space.

15. 16. 17. 18. 19. 20. 21.

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10. I promise to diligently assess the soft tissues of the cervical, thoracic and lumbar spine (as well as extremities) before making the statement no soft tissue abnormality is seen. 11. I promise not to call the smaller disc at L5-S1 as degenerative disc disease unless there are associated osteophytes. 12. I promise not to call the small discs of the lower thoracic spine on a lateral lumbar film as degenerative disc disease. KUB is useful when you suspect these diagnoses: perforated viscus, intestinal obstruction, adynamic ileus, abdominal abscess, bowel infarction, fat versus ascites (obese patient), emphysematous cholecystitis and colitis, gallstone ileus, urinary tract calculi, abdominal aortic aneurysm.

95

The difference between the KUB vs. Lumbar films: KUB uses 80-90 kVp, 40 FFD, and CR is 1-2 below the iliac crest. The Lumbar view has a kVp of 75-85 kVp, otherwise, they are identical. The collimation is wider for the KUB. There are three additional views; there is a KUB erect (upright) view, KUB decubitus and KUB oblique view. They are taken to see how the air moves around. When doing an erect AP Abdomen study, the changes you will find from being in the erect position include: Air fluid levels (air rises and fluid sinks, it is normal to see small amounts of air- fluid levels) Kidneys drop Small bowel and transverse colon drops Breasts drop Lower abdomen bulges and increases in density in the lower 1/3 Diaphragm descends

Abdomen
Note: SB = Small bowel, and LB = large bowel. Ok now onto one other point. I added some info from other places into this review. Theres some information from LearningRadiology.com. I also suggest looking at some cases on mypacs. I have also included a few links to some powerpoint presentations from LearningRadiology. I found them very helpful, myself. They go through things a bit differently than we did in class, but it helped make sense of SBO/LBO/Adynamic Ileus. The only difference is that LearningRadiology separates Focal from Generalized Adynamic Ileus. There is also a powerpoint for abnormal air in the abdomen, calcifications and abnormal masses in the abdomen. There are quizzes and things at the end with answers, so I suggest going through them all. Its good practice!

Imaging Techniques
KUB recumbent view The basic abdominal view, an x-ray showing the kidneys, ureter, and bladder. Doesnt show us these structures. Patient lies supine, and the KUB will show the entire abdomen. The films will read as if the patient is facing you, so the left upper quadrant is on the upper reading right. The abdomen view is wider than a lumbar spine film. You should be able to see the flank stripes bilaterally (fat right along the wall of the peritoneum, if not seen bilaterally, could indicate inflammation), the hemidiaphragms superiorly, the symphysis pubis inferiorly, and the sift tissues and the gas shadows in the large bowel. It is normal to see a have gas in the large colon, but you should not have a lot of gas in the small intestine (a small amount is ok). If you do see gas in the small intestine, know that the small bowel is located more centrally, and the large bowel is located more peripherally, and picture frames the small bowel. The KUB image is constantly changing since the gas is always changing. Gas is more prominent in the descending colon as opposed to the ascending colon. When the feces are in the ascending colon, there is a lot of water mixed in with it, making it more diarrhea-like (with less space for air). By the time the feces get to the descending colon, a lot of the water has been absorbed, therefore making more room for air/gas bubbles.

Barium studies Upper GI study: The contrast is not always appropriate (ex: in the case of perforation). A metallic density is injected into the patient to fill the lumen of a structure in the GI tract, then an x-ray is taken to Indications for a KUB film see any irregularities, Abdominal pain (moderate to severe) obstructions, masses or defects. Abdominal pain + significant tenderness Timed studies can give Trauma functional information regarding motility of the bowel. Abdominal distention Pain, vomiting, diarrhea and constipation However 3-dimensional information is not available as it is with CT. Lumen of the structures can be evaluated for filling defects, mass effects, and irregularity of the lumen wall such as ulceration. Barium studies are not being used as much any more because CT is becoming more readily available. Barium Swallow: The barium contrast (metal density, should be whiter than bone) is given orally, resulting in imaging of the esophagus. You can also see the upper GI and a small bowel follow through (you can time the radiographs to see the stomach, the small bowel).

 Barium Enema: A procedure in which barium sulfate is introduced into the intestine through the rectum where it will travel through the large bowel and stop at the iliocecal valve. Air Double Contrast Study: Give the patient barium, then push air through the large colon. They are great when there is suspected abnormalities, tumors or masses extending into the bowel lumen from the wall.

96 MRI Provides information about solid, immobile organs, such as the liver and kidneys. Mobility of the abdomen contents degrades the image quality, so CT is better in this case. MRI is not very good at for viewing calcifications either. Can be done saggitally, axially or coronally. Great for the liver, spleen, lungs, uterus, etc.

ABCs & Reading the FIlm

Air: Assess gas patterns (distension, displacement). Look for normal and abnormal IVP intralumenal and extralumenal gas. Describe its appearance, location, displacement, AKA: Intravenous pyelogram. Normally, the Air in Small Bowel Air in Large Air in Rectum/Sigmoid and distention. Normally, there is ureters are difficult to visualize completely always air in the stomach Bowel Colon because of the peristaltic waves pushing the (meganblasse). In a non-distended Localized Yes - 2-3 distended loops Yes - Air in rectum Yes contrast. Contrast is injected intravenously small bowel, there will be 2-3 loops, Ileus or sigmoid into the patient. The contrast travels through with a normal diameter of 2.5 cm Generalized Yes - Multiple distended Yes Distended Yes the blood stream, and then exits the body via (about the size of a US quarter!). In Ileus loops the kidneys, ureter, bladder, etc. The size and the large bowel, it is normal to see air SBO Yes - Multiple dilated No No shape of the kidneys become apparent, as do in the rectum and sigmoid colon, loops the ureters, and the bladder. You cannot see a almost ALWAYS. There are two types LBO No - Unless ileocecal valve Yes - Dilated No whole lot of the urethra in this study, only the of abnormal gas patterns: functional incompetent very top part of it just beyond the bladder. ileus (local or generalized adynamic The ureters may appear to be missing at certain parts, but this is normal. There is a ileus), or mechanical obstructions such as an LBO (large bowel obstruction) or SBO (small peristaltic activity to the ureter, and a muscular area around it, which can make the bowel obstruction). This was a ureter appear to have disappeared. It is not normal to see an abnormal expansion of the ureter surrounded by normal ureter widths. handy dandy little chart off learning radiology that I thought I would include. Its handy- In the barium enema, the solid organs are not well seen. But in the IVP, you can actually see the kidneys, ureter and bladder. Diagnostic Ultrasound We are not going to be taught about it, but we will learn when it is indicated. Diagnostic US is non-invasive, non-ionizing, and highly available. It will show most abdominal organs, except gas filled bowel. It allows the clinician to measure masses and determine matrix. The most common organ to use Diagnostic Ultrasound is the gallbladder. It is also commonly used to find calcifications, but is not used for examining the GI. CT CT provides greater detail, and can be used with or without contrast (vessels, GI). The exam time is longer in CT scans, and axial images can be obtained. You can take measurements from a CT scan, and you will be able to see all structures (muscles, kidneys, feces, air-fluid levels, calcifications). CT is great at picking up calcifications. dandy-indeedy. It was NOT presented in class so take it or leave it. I thought I would include it.

So what does this chart mean? It means that if you see air everywhere, with the SB having 2-3 distended loops, you should be thinking localized ileus. If you see air everywhere, but the SB and LB are both distended, think generalized ileus. If you see dilated loops of air ONLY in the small bowel, think of an SBO (because air cant get past the point of obstruction). Finally, if you see dilated loops of air only in the large bowel, think LBO. If you see an LBO (so dilated loops only in the large bowel), there should not be any air in the small bowel as well in an LBO because the ileocecal valve stops it. However, the ileocecal valve sometimes malfunctions, in which case you can see air in the SB as well. Here are some great examples of some of these conditions: http://www.learningradiology.com/notes/ginotes/pictorialbowelgas.htm.

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Here is another powerpoint from learning radiology called Recognizing SBO, LBO and Ileus: http://www.learningradiology.com/medstudents/recognizingseries/recogobstru ctflashpage.htm And another called Recognizing Abdominal Calcifications: http://www.learningradiology.com/medstudents/recognizingseries/recognizea bdocalcflash.swf One more called Recognizing Abdominal Soft Tissue Masses: http://www.learningradiology.com/medstudents/recognizingseries/recogmasse sflash.swf And just one more Recognizing Free Air: http://www.learningradiology.com/medstudents/recognizingseries/recogfreeai rflash.swf

Bone: Check for calcifications (patterns, locations). Are there any calcifications that should not be there? Cartilage. Theres not a ton to look for in terms of cartilage on an abdomen film. Check out the IVDs, and the symphysis pubis. Look to the hip joints, SI joint, all those fun areas. Soft Tissues. Look at the organs. Where is the problem? Localize the problem to the four abdominal quadrants, or is it in the pelvic region (which is not included in the four quadrants). Is the organ peritoneal or retroperitoneal? Determine this on the lateral view. Is there a density in the organ? If so, where does it extend? Is there fat outlining the organ? Is there a mass effect (air shadows being pushed away because of a growing mass)? A note about fluid levels: it is normal to see fluid levels in the stomach (always), except if the patient was supine with radiographed. You may see 2-3 levels in the small bowel, and you should not see fluid levels in the large bowel.

97 RUQ: LUQ: Small bowel Small bowel Liver and Gallbladder Left lobe of liver Pylorus Spleen Duodenum Stomach Head of Pancreas Body of pancreas Hepatic flexure of colon Splenic flexure of colon Portions of ascending and transverse Portions of transverse and descending colon colon Right adrenal gland Left adrenal gland Portion of right kidney Portion of left kidney RLQ: LLQ: Small bowel Small bowel Cecum and appendix Sigmoid colon Portion of ascending colon Portion of descending colon Lower pole of right kidney Lower pole of left kidney Right ureter Left ureter Soft Tissues Seen on X-Ray Soft Tissues Not Seen On X-Ray Stomach Pancreas Psoas Shadow Gallbladder Large Bowel Small intestine Kidneys Uterus Bladder (If full enough) Prostate Gland Liver Spleen Hepatomegaly/Liver Enlargement Normally, the liver should extend just inferior to the costochondral margins and it should be very pointy at its inferior border. The tip is allowed to come below the iliac crest, but it has to be pointy in order to still be normal. If the tip at the inferior border is blunted and curvy (not pointy) this indicates pathology. The liver should not shift across midline, and it should not extend inferiorly past the iliac crest. Also, look to see if the liver is wider superiorly and causing any displacement of bowel gas/other structures. There is normally bowel gas in the RUQ so it you dont see any, this could indicate a large liver. The enlarged liver will cause displacement of other organs on the film. Often times, you will not be able to see the outline of the liver itself, so you must resort to looking at the surrounding structures, such as the hepatic flexure of the colon and where its located, etc. Radiographic Findings: The liver projects below the costal margin (not reliable). Downward displacement of the hepatic flexure. Stomach displaced left and backwards (seen best on lateral view, especially if theres lots of air in the stomach). Right kidney

Organ Enlargement/Displacement, Anomalies, & Abnormal Abdominal Air Patterns

 often displaced downwards.**Lower edge of the liver crosses the right Psoas shadow (This is the most reliable sign: i.e. if the liver projects medial to the psoas shadow). Possible elevation of the right hemidiaphragm (only if the liver is huge). Bowel gas displaced down and medially. Large homogenous water density in RUQ. Clinical Significance: Clinical information helpful; ask how much alcohol your patient drinks (alcoholics), if theyve ever had cirrhosis, past history of cancer or heart problems, bruising, or nutritional problems. Causes of Hepatomegaly: Pringles List of Causes (similar): Anemia Lymphoma Leukemia Tumor (Hepatoma/Mets)* Infection + Alcoholism and Cirrhosis
nd

98 Splenomegaly/Enlargement of the Spleen The spleen is in the LUQ, just below the left hemidiaphragm. Sometimes you may see an elevated hemidiaphragm, but this is not common. This can happen in conjunction with liver enlargement so a patient can have hepatosplenomegaly. An enlarged spleen is commonly caused by: lymphomas*, leukemias*, anemias*, mononucleosis, parasitic infections, or cirrhosis. (*These are the big three). Pringle gave another set of causes, which are similar but easier to remember because of the acronym (ALL TIT): Anemia* Leukemia* Lymphoma* Trauma Infection Tumor

Fatty liver (alcoholism/cirrhosis) Cancer (hepatoma*/Mets* (M/C)) Lymphoma CHF Hepatitis Hemolytic anemias Metabolic storage diseases Osteopetrosis.

Radiographic Findings: Medial displacement of megenblasse. Splenic flexure of the colon is displaced downwards. Left kidney pushed downwards and medially. If there is very significant enlargement of the spleen elevated hemidiaphragm. Large homogenous water density in the LUQ. Spleen extends below costal margin. Bowel gas displaced inferiorly. Management: Send the patient back to the GP for further investigation. Kidneys Conditions On x-ray, we can see the kidneys pretty well because they are covered in fat. You may also notice in some people, that the left kidney is a little bit higher than the right. This is a normal variant, and occurs because the liver sits on top the right kidney, pushing it down. The kidneys should be parallel with the psoas muscle (shadow), and should extend 3 vertebral segments (usually T12-L3). You will likely not see the ureters because they are surrounded by smooth muscle (for the function of peristalsis). If you see distension proximal to the ureters, you can assume that there is backup (and possible enlargement). This should guide you to look for things that can cause urine backlog such as calcifications, congenital causes (abnormalities to the kidneys, ureters (bands/strictures) or masses). IVP is the best way to see the kidneys, but involves contrast (which isnt so good). When describing the kidneys, always note where you see the increased density (i.e. what quadrant), and compare with the lateral view to see where the issue is (retroperitoneal or intraperitoneal). After youve cross-triangulated, you should be able to tell what organ the increased density is from, which will lead you to a list of

(NOTE: Trauma is not included in the list!) So the acronym is ALL TI (minus the 2 T). Also Note: Sometimes you can get a normal-sized liver with a long and thin area extending downwards towards the ilium. If the liver doesnt displace any of the air in the bowel, or any other structures on the x-ray, this could be a normal appearance. This is why seeing the liver projecting below the costal margin is not a good way of determining hepatomegaly. If you cant see the borders of the liver (and you may not), look to the air shadows; find the hepatic flexure and the colonic air shadow, find the fat outline of the kidney shadows. Depending on whether these are in place or displaced can help you decide if hepatomegaly is present. You only may see some air density in the area of the RUQ where the hepatic flexure is.

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differentials based on the organ, patient age, radiographic findings and clinical presentation. Common causes of unilateral kidney enlargement: Congenital: Hyperplasia (usually associated w/ hypoplastic opposite kidney), or agenesis of one kidney (very rare) Genetic: PKD (Polycystic Kidney Disease, usually bilat) Obstructive hydronephrosis* Neoplasm (Wilms Tumor, Renal Cell Carcinoma, Metastasis) Obstructive hydronephrosis = Water in the kidneys is causing a blockage. This is the second most important to rule out. Neoplasms of the kidneys include: Wilms Tumor, Renal Cell Carcinoma or Mets.

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Horseshoe Kidney This is the most common anomaly seen with the kidney. The two kidneys will be joined at the midline and inferiorly by a fibrous band, making the kidneys look like a horse- shoe. There will usually be two ureters (or even three!). Can be picked up on lumbar plain films. The kidneys will be fused anterior to the spine. Lower poles will be fused at the midline (looks like a right side up U). Other anomalies (ureters, collecting ducts). The kidneys collecting systems dont drain properly which leads to chronic stones formation, obstruction and chronic infections (UTIs). Note that skeletal anomalies such as blocked vertebra, hemi-vertebra, and butterfly vertebra are linked with visceral anomalies so if you see one of these anomalies, look to the organs Pelvic Kidney Kidneys located down in the pelvis w/ a short ureter. If a patient has kidney surgery, then they may put the kidney in the pelvis. Malrotation of a Kidney We looked at a case of this, but there wasnt anything mentioned. Just know it can happen. Crossed Ectopy Two kidneys on the same side of the body. When a person has a kidney transplant, the donated kidney is put in the pelvis, not in the same spot as the original kidney b/c the kidney is much more supported in the pelvis. They dont even take out the bad kidney, they leave it there. Duplication of the Collecting System Some duplications include: 2 ureters, 2 renal pelvises, 2 set of calyxes. Usually, duplication causes no problems. Once in a while the ureters do not enter the bladder in the proper location and this causes the patient to be more prone to obstruction and infection.

Common causes of bilateral kidney enlargement: PKD (polycystic kidney disease usually bilateral) Acute glomerulonephritis Lymphomas/Leukemias

Kidney Enlargement Kidneys usually extend 3 vertebral bodies plus disc spaces, and they normally are oriented parallel to the psoas shadow. Causes of unilateral kidney enlargement (GONC): Genetic (PKD). Obstructive Hydronephrosis*. Neoplasm (Wilms Tumor, Renal Cell Carcinoma or Mets)** (Most NB to rule out). Congenital hyper/hypoplasia/agenesis. Causes of bilateral kidney enlargement PAL: PKD (congenital, hereditary, develop larger kidneys over time and eventually lose renal function). Acute glomerulonephritis* Lymphoma & leukemias* (may also see enlarged liver, spleen, kidneys and even LN). Radiographic findings: Large homogenous water density in either one of the upper quadrants or both. Retrograde pyelogram: Will be able to see the tubes going into the ureters; used to look at the structure (not the function) of the kidneys. (In polycystic disease, the collecting systems are bizarre and are too big. They will be very stretched; pts will have a hx of it). Note: Hydronephrosis can be due to kidney stones or an infection. PKD = Polycystic Kidney Disease. Even though this is on the differential list for unilateral kidney enlargement, PKD is usually bilateral. Congenital hyperplasia of one kidney is usually associated with a hypoplastic opposite kidney. This is not that common. Congenital hypoplasia is very rare.

 Obstruction of the Bladder Huge water density in the pelvis extending up to T12/L1. Ex: 74 yr old male with severe LBP and pelvic pain. The problem was caused by the patients prostate. Tx: Catheter to drain the urine, then prostate surgery.

100 LearningRadiology: Dilated colon to point of obstruction, little/no air in rectum/sigmoid colon, little or no gas in the small bowel. If there is gas in the small bowel, there is an incompetent ileocecal valve. Clinical Significance: All obstructions need to go to the Emergency Room due to risk of perforation (call 911). If you think the cause is colon cancer, refer to oncologist.Abdominal distention. Adynamic/Paralytic Ileus This condition can also cause air in the large bowel (as well as the small bowel). See below in the small bowel section of notes. Diverticulitis Outpouchings along the GI tract.

Large Bowel Conditions

The large bowel has a wider lumen/diameter than the small bowel, and is located more peripherally. It forms a picture frame around the abdomen. The large bowel has haustra which are bowel loops that extend 1/3 the diameter across the bowel from each side. The small bowel has what are called vulvulae, which normally extend the entire distance across the SB. Toxic Megacolon This is a life-threatening complication of other intestinal conditions (inflammatory bowel disease and infection) causing sudden widening/dilation of the large intestine within one to a few days. Usually seen as huge gas in the large bowel.

Wikipedia: Diverticulosis is a disease of the large intestine, where there are many pouches (diverticula) coming off the outside of the colon. Diverticulitis is when one of the Radiographic Findings: Huge gas in the large bowel exceeding the 6 cm limit (distention). diverticula gets inflamed. (HUGE large bowels!!!) The transverse diameter of the large intestine should not measure more than 6 cm (although the cecum can measure up to 9 cm). The large Radiographic Findings: CT is best. Chocolate chip sign intestine is very fragile and will easily perforate. Clinical Significance: Wikipedia: Class triad of symptoms: left lower quadrant pain (Im Clinical Significance: Ask the patient if they have ulcerative colitis of Crohns (they are pretty sure that was on the Clinic Entrance Exam), fever, leukocytosis (+WBCs). prone to toxic megacolon).Patient will present with abdominal pain and distension, Patients might have a fever, have diarrhea or they might be constipated. abdominal tenderness, fever, rapid heart rate and shock. High risk of Colon Cancer/Carcinoma in patients who have Ulcerative Colitis/Crohns. Note: The chocolate chip sign was named by Dr. Pringles graduating class. In diverticulitis, there are a lot of little outpouchings along the GI tract. When the patient Note: Ulcerative colitis is located throughout, whereas Crohns is more patchy. Ulcerative has a study done and they inject contrast through the bowel, some of this contrast will Colitis/Crohns Toxic Megacolon or Colon Cancer. get stuck in the little diverticuli. The result are many little contrast densities that literally look like Chipits Chocolate Chips! How fun! LBO/Large Bowel Obstruction Causes: Crohns Disease/Regional Enteritis Colon carcinoma** Diverticulitis** Cecal volvulus Peritoneal metastasis Massively distended bladder/pelvic mass Pressure from external structures Adhesions Wikipedia: Crohns is an inflammatory disease that can affect the GI tract anywhere from the mouth to the anus. Thought to be of autoimmune origin, where the GI tract is attacked causing inflammation. Radiographic findings: Strictures cause the bowel to be narrowed. Cannot be evaluated on plain film. If there is a period of inflammation, you may be able to see distention, but thats all youll ever see on plain film. Crohns is more matchy than ulcerative colitis (which is located throughout). Clinical Significance: Wikipedia: Symptoms include abdominal pain, diarrhea, vomiting, weight loss. The patient may also present with skin rashes, arthritis, inflammation of the

Radiographic Findings: Gas in the large bowel, but then no air beyond a certain point (the point of obstruction).

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eye, fatigue and poor concentration. There are no drugs or surgical procedures that will cure Crohns. Treatment only includes controlling the symptoms, keeping the patient in remission and preventing relapse. Note: Inflammatory conditions of the small bowel are large and distended when acutely inflammated but narrow and limp when not in the acute stage. Ascites A ton of fluid in the peritoneal cavity that causes a distended bowel and abdomen. Common causes: Cirrhosis* Pancreatitis Chronic renal failure.

101 any abnormal masses in the small bowels (tumor). Look to the walls of the small bowel. If you can see small little rings around the bowel folds, this is NORMAL. In the large bowel, there are thicker and larger folds (called hoestra). It is not normal to see air/gas in the small bowel. Just to review, the movement of the fecal material flows through the small bowel iliocecal valve ascending colon (cecum) hepatic flexure transverse colon splenic flexure descending colon sigmoid colon rectum. The small bowel is usually 3.5 cm maximum, whereas the large bowel is about 3-5 cm. If we start seeing a lot of air overlying the spine, this usually indicates something going on in the small bowel. If there is a lot of air, there will be areas where the small and large bowels overlap. Complete obstruction can cause air not to extend past the ileocecal valve. If you see air in the small bowel, this indicates three possible differentials: Small bowel obstruction Adynamic ileus Aerophagia (taking in air, usually we release air through burping, but if the air doesnt get released because there has been trauma or the person inhaled deeply or had the wind knocked out of them, this presents as aerophagia).

Radiographic Findings: Air in the small and large bowels (lots in the large bowels) appearing very centrally, with grey areas around the air. The abdominal tract is floating on top of all the fluid in peritoneal cavity. You will not see the large bowels taking the classic loops up, across and downwards, instead, the large bowel will be located more centrally (because the bowels are all floating on top of water in the abdomen). Hence, the air within the bowels is located centrally (floating on top), of the water (greyness) which will appear more laterally. Will only see this on a supine radiograph (not erect). Clinical Significance: Distended Abdomen. Patient needs to have the fluid drained, and the cause of the fluid needs to be determined. The history is very important here! Alcoholism can lead to cirrhosis and pancreatitis. The ascites will hide most of the radiographic signs of this. The other scenario to consider is that the patient is diabetic and is going into chronic renal failure. Send these patients back to their GP for blood tests, liver (serum amylase) and pancreas function testing (test for alcoholism) and kidney function tests (test for DM). If the patient is diabetic, they need a referral to a nephrologist. Note: Will be unable to assess the displacement of the bowels because both the small and large bowel are floating on top of the fluid (and are displaced). Distended stomachs can occur in SBO and LBO (large bowel obstruction) as well as ascites. CTs may be helpful.

If we see an SBO (small bowel obstruction), common causes include: Adhesions** (most commonly) Tumors

NOTE: 3-5 hours after the onset of acute obstruction, gas and fluid accumulate ABOVE the lesion (no gas beyond the obstruction). Multiple (>2) air/fluid levels in the small bowel is an abnormal finding! String of Beads appearance. Abnormal Small Bowel Air The diameter of the small bowel should not be more than 3.0 cm. Causes: Small bowel obstruction* (Causes include adhesions* and tumors) Adynamic ileus* Aerophagia

Small Bowel
The small bowel is located centrally, pictured framed by the large bowel. When looking at radiographs of the small bowel, look at the size and the width of the small bowel. The width of the small bowel itself (the lumen) is smaller than the large bowel. Look if there is any air going into the large bowel (obstructions are common at the iliocecal valve) or

Radiographic Findings: Small bowel gas. Clinical Significance: Auscultate the abdomen (to ddx obstuction and adynamic ileus): no bowel sounds with adynamic ileus).

 Adynamic or Paralytic Ileus This is not a true obstruction, it only simulates a small bowel obstruction. There will be air in both large and small bowels, but can be localized or generalized. Once in a while you can get focal involvement with loss of peristalsis w/ Cholecystitis (localized loss of peristalsis next to gallbladder) or pancreatitis or appendicitis). Can be caused by SIT: Surgery, infection or trauma. Surgery (w/ any abdominal sx, the bowel automatically stops working and will not start again for 3-4 days on its own), infections (appendicitis, cholecystitis, pancreatitis) or trauma (if seen in a patient, take this a clue to look for a fracture). Radiographic findings: The lumen of the small bowel remains patent and unobstructed. The distended segments are short (making them look like they are stacked on top of each other). Loss of peristalsis. Local or generalized. Air in both small and large bowel (because its not a true obstruction). There will be gas in the rectum or sigmoid. Air will be seen beyond the ilium! There will be no obstruction! Clinical Significance: Often associated with trauma and infection (appendicitis, cholecystitis and pancreatitis). IMPORTANT! The bowel will still be patent/obvious. This is NOT an emergency. If it is due to pelvic trauma, determine if the trauma or fracture is stable or unstable. If it is unstable fracture, send them to the hospital by CALLING 911! If they are post-surgical, dont worry about it, just be aware of it. This is a non-emergency situation if it occurs after surgery. No bowel sounds, vomiting and level of pain. Pain is not predominant, abdominal distension may not be as prominent as SBO, absent bowel sounds, and air in the large bowel. Note: Always try to assess where the air is located and use yoru anatomical structures to differentiate. If there is air in the sigmoid colon and rectum, then this indicates there is no blockage in the large bowel. Peristalsis isnt working (there is no obstruction) so the air can still get past the problem. SBO/Small Bowel Obstruction Commonly caused by adhesions after surgery or scarring, and tumors. Typically about 3-5 hours after the onset of the acute obstruction, gas and fluid accumulate above the lesion (no gas will be found beyond the obstruction). More than 2 air/fluid levels in the bowel is 100% abnormal. Radiographic findings: String of beads/slinky appearance (because of inflammation along the wall of the small bowel). Air/fluid levels (>2 abnormal). Air/fluid levels on erect film. Bowel gas looks stacked. LearningRadiology: Dilated small bowel. Little gas in colon, especially rectum. Key: Disproportionate dilation of small bowel. Columbus: Patients who vomit usually have an obstruction higher up. Patients who have constipation usually have an obstruction lower down.

102 Clinical Significance: Need to find the cause of the obstruction. May not see the obstruction, but the patient needs to go to the emergency room right away to figure out the cause and to determine risk of rupture (call 911 based on clinical picture). Advanced imaging such as CT is needed. There is a chance they could rupture. So Call 911! Colicky pain, abdominal distension is prominent, increased bowel sounds and no air in the large bowel. Note: An obstruction = nothing will be able to get past the obstruction (i.e. there will be no air past the obstruction). What is the difference between an SBO and paralytic ileus? They both have air in the small bowel, but an SBO will block air from getting past the point of obstruction into the large bowel, whereas paralytic ileus is just a lack of peristalsis so air can still get into the large bowel. If you see air beyond the large bowel they you know it is paralytic ileus. Causes of paralytic ileus are usually trauma/surgery. Look for signs of pelvic trauma and then choose your plan of management. Gallstone Ileus A gallstone in the ileus. An infrequent cause of mechanical bowel obstruction. Gallstone ileus is caused by an impaction of the gallstone in the terminal ileus by passing through a biliary-enteric fistula (often from duodenum). (So basically according to Karen, the gallstone eroded through the gallbladder and entered into the small bowel. Thanks Karen!) From here, it takes a tour downwards, where it gets stuck around the ileocecal valve in the pelvic inlet. (However, it can get stuck anywhere). Radiographic Findings: Signs of partial/complete intestinal obstruction, air in the biliary tree (pheumobilia), direct visualization of the stone, change in position of a previously located stone, and two adjacent small bowel air-fluid levels in the right upper quadrant. Tell-tale sign: AIR IN THE SMALL BOWEL.

Gallbladder
Air in the Biliary Tree This is ALWAYS abnormal! (Fistula (hole) in GI tract). It can be caused by surgery to gall bladder, gall stone ruptured into the small bowel* or malignant tumor* (*be worried about). Radiographic Findings: Streaky air pattern in the RUQ towards the liver (black streak in RUQ). Lots of air in the small bowel. Clinical Significance: Middle aged female w/ increasing LBP and stiffness, possible hx of gall bladder removal. Possible surgery allowing air in the biliary tree, or possibly gallbladder is pathological and a stone ruptured allowing air in, or a malignant tumor

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pressed against the structure and caused necrosis. Causes fistula in the GI tract (an abnormal connection between the biliary tree and GI tract. Emphysematous Cholecystitis Gas in the gallbladder (rare, we likely wont see this). Radiographic Findings: Oval lucency in the RUQ (air in the gall bladder wall that never moves). The large bowel will likely be displaced!! Clinical Significance: Patients will likely have poorly controlled diabetes (insulin dependent) and will complain of RUQ pain. Also seen in acute infection of the gall bladder caused by a gas-forming organism. Tx: Surgery. Some notes from Peterson:

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Ovaries
Ovarian Carcinoma Radiographic findings: Huge water density in the pelvis. Clinical significance: Poor prognosis. Middle aged females w/ insidious onset of increasing LBP, and a huge mass in the abdomen on palpation.

Pneumoperitoneum
Air under the RIGHT hemidiaphragm due to ruptured duodenal ulcer (air outside the GI tract). Radiographic Findings: You will see air just under the hemidiaphragms, the air takes on the shape of the hemidiaphragm. You may see bowel in the air space. We cannot see the flanks because they will have become obstructed. According to learningradiology, you will also see air on both sides of the bowel walls, if theres air in the peritoneum. Clinical Significance: Conditions causing extraluminal air: recent laparotomy (lasts 3-7 days)*, trauma (iatrogenic or severe external forces)*, or a perforated abdominal viscus (gastric or duodenal ulcers)*. Other causes include abscesses (subphrenic and other), biliary fistula (possibly due to stone formation), cholangitis, pneumatosis coli (source of infection in the bowel itself), nectrotising enterocolitis or portal pyaemia (infectious cause).

You should worry about air in the portal venous system due to an infracted bowel. In the supine position, depending on how much is present, the gas in the stomach will rise anteriorly to outline variable volumes of the body and antrum. The resting gastric fluid will form a pool in the fundus beneath the diaphragm, posteriorly on the left-hand side, creating a circular outline. The mass will disappear by turning the pt prone or making them sit upright (itll then appear w a fluid-level directly beneath the medial aspect of the left hemidiaphragm). Gas in the small bowel is not normal in a healthy, ambulatory adult; but when it is present, itll appear as coiled, spring-shaped folds that cross the entire lumen. The transverse measurement should not exceed 2.5-3.0 cm, increasing slightly distally. The classic anatomical layout of the colon is often found to be deviated from by tortuous and redundant bowel, but the hepatic and splenic flexures should be identifiable as the highest fixed points on the right and left sides, respectively. The transverse colon may dip down deeply into the pelvis, but the fecal content of the bowel becomes increasingly solid and formed as one passes distally, eventually generating discrete masses which may be individually identified, but which always containing many tine pockets of gas.

When visible, the haustral folds of the colon may be seen, only partially visualized across part of the large bowel lumen, although in some patients complete crossing of the lumen by haustra may occur.

Intra-Abdominal Calcifications and Other Interesting Densities

Approach to abdominal calcifications: Identify the calcific pattern. Localize the findings anatomically. Develop a differential diagnosis.

Normal structures that calcify: Costal cartilage Mesenteric lymph nodes (are every/anywhere) Pelvic vein clots (phlebolith) Prostate gland

Colostomy Stoma
Radiographic Findings: Radiopaque part in LUQ. Clinical Significance: They reroute the large bowel to the abdominal surface. Its a way in which the patients can control their bowel movements.

Abnormal structures that contain calcium (where the calcium indicates the pathology):

 **Calium indicates pathology Pancreas Renal parenchymal tissue Blood vessels and vascular aneurysms Gallbladder Fibroids (leimyoma) Biliary calculi Renal calculi Appendicolith Bladder calculi Teratoma abnormal structure such as a tumor). Will see a rim of calcification around it. Ex: Porcelain Gallbladder. Examples: o Simple cysts o Aneurysms o Echinococcal cysts o Hematoma o Porcelain gallbladder (gallbladder that has become calcified) Solid mass Conduit wall: within a tube or a vessel.

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Concretions
Gallstones (Choleliths), Cholelithiasis (Concretions) Seen only if there is enough calcification (15-20%), therefore, most stones are not visible on plain film. The gallbladder may be located as low as the PSIS. Variable in size. There are two types: cholesterol or bile. Risk factors: hemolytic anemia, liver cirrhosis, diabetes, or transplants. Radiographic Findings: US is the modality of choice. Calcify densities in RUQ where the outer rim is dense, the centre is more lucent (mixed stones, calcium and cholesterol). Maybe laminated and faceted if there are numerous layers. Stones can be seen as low as the PSIS. If the gallstone erodes the wall and enters the small bowel, it can travel through the small bowel (look for air in the biliary tree from surgery or erosion of the gallstone). If it travels through the iliocecal valve, they can appear in the RLQ. Most are not visible on x-ray, you can only see then if they calcify (which takes a long time). Clinical Significance: Symptoms arise when they eat fatty food. But the patient may or may not even have any symptoms. More common in women over 40. Check for familial history. Refer to an internist for removal of the gallbladder. May have symptoms, may not have symptoms. When they are confined in the gallbladder, they are found in the RUQ. Only 10-15% of gallstones calcify, and this usually occurs in females who are fat, forty and fertile (The Four Fs). Note: Milk of Calcium: is a sequelae of Cholecystitis. Calcified biliary sludge (bile within gallbladder) within the lumen of the gallbladder. Associated with gallstones in 90%. This is not a common occurrence. Must differentiate this from a contrast technique (so ask the patient if he/she has had a contrast image done recently. These stones are more round. Phleboliths Deposits of calcium in the wall of a vein. Common in the pelvic area. Generally asymptomatic and harmless. May be associated with enlarged bladder, rectal distension, diverticular disease, stomach carcinoma and other tumors. These may look like a stone

There are Four Patterns of Calcification: ADD IN INFO FROM BELOW, OR MAKE THIS INTO A CHART! Concretions: form within a hollow structure. Vary in appearance from lucent centre with minimal calcification to dense calcification with detailed layers. Varied shape (round, oval, faceted, unique shapes), borders (sharp, well defined, continuous/uninterrupted), variable internal appearance (laminated, homogenous, lucent centre, etc). Concretions can also have a variable appearance internally, they can look laminated, homogenous, have a lucent center, etc. You will most often see concretions within structures that have lumens rather than solid organs. Examples: o Gallbladder (gallstones/choleliths). These may look like multiple small individual stones. They may appear faceted because they are rubbing up against each other and this is very typical of stones in the gallbladder. o Urinary tract (renal, ureteral or bladder calculi) o Diverticulum/Appendix (fecalith, appendicolith) o Pelvic veins (phlemoliths) o Pancreas (calculi) o Prostate (calculi) Cyst Wall/Cystic Calcification Calcification in the walls of a structure. (Note, this has nothing to do with the presence of a cyst, it just describes the pattern of calcification). It will appear round or oval shape, like an Easter egg. Calcification in the wall or a structure or mass such as a cyst, pseudocyst or aneurysm. Tyically seen when the walls of a solic organ becomes calcified, making the outside look darker/calcific, and the inside more lucent. Smooth curvilinear rim of calcification is seen. Appearance: round/oval, smooth, curviilinear rim, rim calcification generally continuous, margins are sharp and the interior is less dense than the margins. Will not see any facets, or laminations as with concretions. They are forming within a solid structure (existing solid organ such as liver, spleen or kidney, or it can occur in an

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in the ureters. One of the concerns, if its located near the ischial spine, is that the stone is a renal calculi. These stones could be the cause of a patients LBP. Fecolith/Appendicolith RLQ. Fecolith = anywhere along the tract. Appendicolith = if you think its in the appendix. Radiographic Findings: Solitary, rounded concretion in the RLQ. Will be near the ascending colon, medially. Can be quite large. US is great for seeing these. Clinical Significance: Risk of rupture. Seen in 10% of acute appendicitis. Seen in 1/3 of removed appendix cases. Ask if the patient has a history of appendicitis. Calcified Lymph Nodes Primarily Mesenteric Nodes in the RLQ or lower central abdomen. Causes: Prior infection (TB or Histoplasmosis). Radiographic Findings: Popcorn-like density of 1-1.5 cm in the RLQ or lower central abdomen. In the neck = calcified cervical lymphatic chain. Popcorn densities in the left quadrant = Mesenteric Lymph Nodes. Clinical Significance: Due to previous infection (TB or histoplasmosis). Splenic Artery Calcifications Splenic artery is the third most common artery to calcify. Patients can get aneurysms of the splenic artery but they barely rupture. The splenic artery calcifications are more common in women, whove had natural deliveries. Radiographic Findings: Snake-like (S-shaped) tubular calcifications in LUQ. Calcification of the Abdominal Aorta and of the Common Iliac Artery Common iliac artery bifurcates at antero-inferior margin of L4. Radiographic Findings: Tubular calcifications in a linear pattern (arterial calcifications). Clinical significance: Elderly or 40 YOM. Clinical significance of abdominal aorta calcification: arteriosclerosis. Does the amount of plaquing seen on the x-ray correlate to the loss of blood flow to the lower limb? No. You might see a lot of calcification in one patient with good flow, and another patient with very little plaquing might have severe vascular caludication. Its not about the calcification, its the amount of fat depositied in the lumen thats the problem. There is a correlation between cigarette smoking and calcification of arteries. Note: Veins do not calcify = theres not enough pressure!

105 Monkeburgs Medial Sclerosis A form of arteriosclerosis where its not the intima layer involved but the muscular layer (media) is. Commonly seen in diabetics. Radiographic Findings: Concentric rings that were stacked up on each other next to the femoral shaft medially (thats how we know its in the media). Aneurysms Clinically silent until something horrible happens. One of the reasons why patients over 65-50 yrs more likely need to be x-rayed, always rule it out first! In the abdominal aorta they rupture. In the thoracic aorta, they dissect (blood goes between the layers of the artery). Radiographic Findings: Only about 50% of all aneurysms have enough calcifications in them to see on x-ray. Surgically, they all have calcifications. Walls of the abdominal aorta are not parallel, theres ballooning and divergence of vessel walls. Transverse diameter of the aorta is >3.5 or 3.8 cm. Anterior scalloping/pressure erosions (Oppenheimers erosion) of the vertebral body due to pulsations of abdominal aortic aneurysm (rarely seen). Diagnostic US is the imaging modality of choice for detecting AAA once suspected on plain film. If a rupture is suspected, a CT is done. Clinical Significance: Asymptomatic elderly pt, pt with LBP that cannot be reproduced. Most pts dont have a palpable abdominal mass (b/c the aneurysms are full of clots which dont transmit the pulsations). Tx: Surgery. Note: If you miss this, you can get sued! Ddx for anterior scalloping is HL (enlarged LN). Ruptured AAA On CT, this causes the right kidney not to be in its correct position and to be surrounded by blood. Refer to ER immediately for surgery. Radiographic Findings: Curvilinear calcification to the left of the spine superimposed over the psoas shadow. Clinical Significance: Excrutiating LBP, hypotensive. Recommendations for AAA: between 3.8-5 cm = Refer to the GP (they dont grow quickly so its not an emergency). >5-6 cm: refer to the ER (they grow more quickly). Outline the aneurysm when you refer to the GP since they usually cant see them. Ruptured Thoracic Aortic Aneurysms This aneurysms dissect (blood goes between the layers of the artery).

 Calcific Foci in the Liver and Spleen Healed foci of previously widely dissemination infection: TB, histoplasmosi, Brucellosis, fungal infections. If in the spleen only, include Hemangioma in DDx. Radiographic Findings: Stippled calcific densities in LUQ ( = spleen). Dermoid Cysts in Ovary (Teratoma) 10% of all ovarian cysts are dermoid cysts, and they are not a product of conception. Teratoma contains calcified or incompletely formed teeth, fat or hair (contains all 3 germ layers). These are located in the ovary, not the uterus. Radiographic Findings: Abnormal (molar shaped) calcific densities near left ischial spine. Clinical Significance: Patient may present with pain. Treatment will refer to gynecologist because they can get quite big. Can be rare to malignant, most are benign. Can cause pressure on adjacent organs (patient may present with pain). Uterine Fibroid Radiographic Findings: Amorphous mass, mulberry appearance in the pelvis. If it extends out of the pelvis and theres displaced bowel gas = huge fibroid. Clinical Significance: 50% of females over 50 have them. Can cause pain, bleeding, sciatica, and most are asymptomatic. When you see one, go to the history and make sure the patient has not had a hysterectomy. Note: Dont confuse fibroids with calcified fecal material which is very rare and youd also have severe constipation. Adrenal Calcifications Not that common. Have to DDx from kidney calcifications since both are retroperitoneal (adrenals sit on top of the kidneys). If its in the adrenal gland, itll be a small region and very, very close to the upper lumbar or lower thoracic spine. If its in the kidney, it will be in a bigger area. Radiographic Findings: Stippled calcific densities in a small region very close to the upper lumbar spine or lower thoracic spine. Calcification patterns: If the calcification is Intralimina, stones in the kidney is called nephrolithiasis. If the calcifications are intraparenchymal, the condition is called nephrocalcinosis. Pelvic calcifications can outline the pelvis of the kidney. Causes: Old TB, Addisons (1/3 of pts), birth hemorrhage (baby who had traumatic birth w/ bleeding into the adrenal glands), or idiopathic. Note: These are in the duct portion.

106 Pancreatic Calcification Calcifications are never normal to see in the pancreas. Normally, concretions occur in organs with a lumen, and the pancreas is a solid organ, but calcifications cau occur in its ducts. If you see calcifications in the pancreas, this is a sign of chronic pancreatitis. Causes: associated with chronic pancreatitis, alcohol abuse (#1 reason), diabetes mellitus (#2 reason), HPTH, pancreatic tumors (rare). Chronic pancreastitis. Radiographic Findings: Stippled calcific densities that follow the spine and trail on up, superimposed over the stomach, in the area of the pancreas). Will be faceted, and more lucent in the center! Will be just tucked up underneath the liver. Make sure theres no air in the biliary tree. (These wont really be stone-like, they will be more stippled and in the shape of the pancreas). Clinical Significance: Chronic pancreatitis is a progressive glandular destruction, fibrosis, and loss of endocrine and exocrine function. This is more common in men 40-50 years of age. Chronic pancreatitis is associated with excessive alcohol abuse. 2-50% mortality after 25 years of the disease. These patients wil have recurrent attacks of abdominal pain. Note: Progressive glandular destruction, fibrosis and loss of endocrine and exocrine function. More common in men. 40-50 YOA. Associated with excessive alcohol use. 25- 50% mortality after 25 years of disease. Destruction of pancreas. Clinical: recurrent attacks of abdominal pain. Get the patient to stop drinking, otherwise the condition will not improve. Complications: pancreatic pseudocysts, biliary obstruction, mesenteric vein thrombosis and pancreatic cancer. Treatment: manage the cause, pain and endocrine and exocrine failure. Porcelain Gallbladder/Cystic Calcification Calcification of gallbladder wall, rare. Obvious signs of diseased organ. Sequela to chronic cholecystitis. 5x more common in females. Radiographic Findings: Calcification of gallbladder wall. Clinical Significance: High incidence of gallbladder cancer/carcinoma. Refer these patients out to an internist for gallbladder removal (cholescystectomy) because of high cancer risk. Often asymptomatic. Note: Dont mistake for calcified costal cartilage. *This is the one exception to the cystic calcifications it is occurring in an organ here! Urinary Calculi Intraluminal solid particles within the urinary system.

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Symptoms may include pain, nausea, vomiting, hematuria and possible fever, chills, diagnostic testing includes US, non contrast x-ray and CT. Treatment includes analgesics, antibiotics, lithotripsy and endoscopic surgery. If you see a stone medial to the ischial spine in line with the ureters, it could be coming down th eureter and into the bladder. If the calcification is below the ischial spine or far medial then this would simply be a phlebolith. Calcium stones would sink to the bottom of the bladder, and would not float on top. Calcifications in the Kidney Kidney stones are very common in the kidney, and there are two main locations for them to be: 1.) In the renal pelvis (calculi formed in calyces). 2.) Parenchyma (functional part of kidney). 3.) Cortex (not common here). There are two types of calcifications in the kidneys (see the next 2 conditions). 1. Calcification in Parenchyma (Nephrocalcinosis): When stones are located in the parenchyma (functional part of the kidney). 2. Calcification in the renal pelvis are called nephrolithiases. Radiographic Findings: Calcification in the Renal Pelvis (Nephrolithiasis): At least 80% of kidney stones are opaque (different from gallbladder). Kidney stones are located retroperitoneally and may be very tiny. Oblique view helpful to see since the stones are retroperitoneal. Clinical Significance: Kidney stones become significant when the patient has signs/symptoms, and the patient wont know if they have stones until there is complete obstruction. The patient will present with colicky flank pain, and radiating pain to the groin, and nausea. Be concerned of the stones getting trapped. Need to differentiate from phleboliths. DDx: benign cysts (younger patients), renal cell carcinoma (in older patients), and hydatid cysts (exposure to infected animals). Note: Dont mix up staghorn calculi with a contrast image, they can look similar. Staghorn calculus: stone increases in size to form a cast of the collecting system due to chronic urinary stasis or infection (looks like an IVP) and it can be bilateral. They look like the horns of a stag, and these are commonly made of struvite. We may or may not see them (only if theres calcification). These patient will have a history of recurrent UTIs from high pH in urine. Look in the pelvicalyceal system. Affect kidney function. Risk of sepsis. Often affect kidney function and can cause infection, sepsis and kidney malfunction. If they arent removed, then the kidney could fail and recurrence could happen. Refer to nephrologist. Nephrocalcinosis Nephrocalcinosis can be cortical or medullary and have many underlying causes. Causes of Nephrocalcinosis (from increased serum calcium):

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HPTH Hypervitaminosis D Cancer w/ bone mets (bone is being destroyed and Calcium is being transferred into the blood). Sarcoidosis (the great mimic) MM

The history is the main thing to look at here. Nephrolithiasis Calcification within the luminal areas with 80-90% occurring in the urinary tract. These take on a retroperitoneal location and they have a risk of rupture. 85-90% of urinary tract calculi contain calcium. Retroperitoneal location, risk of obstruction. Causes of Nephrolithiasis: HPTH (when the pt has their first kidney stone, check for HPTH via serum calcium), Multiple Myeloma, Lytic mets, leukemia, Gout, Tums/Coffee, Genetics. Kidney stones can get trapped over the ileum and down at the ureteral-vesicular junction. Calcium oxalate stones are the most common form of kidney stones. Pain referral for kidney stones will occur from the flank down towards the groin. Bladder Stones Due to chronic urinary stasis or chronic urinary infection. More common in males (because of prostate hypertrophy). Causes: urinary bladder outlet obstruction, recurrent bladder infections ,neurogenic bladder, foreign bodies (catheters). Radiographic Findings: Laminated lucencies in the bladder. Smooth or irregular edges. Clinical Significance: Increased risk of bladder cancer. Symptoms: pain, dysuria, frequency, hesitation, hematuria, or asympatomatic. Tx: surgical removal with or without lithotripsy. DDx List for laminated lucencies in the bladder: Bladder stones Supplements pt is taking

 Suppositories Note: The stones will have come from the kidney, and may have gotten stuck in the lower part of the bladder, where they build, and grow to be very large! Prostate Calcifications Calcific stones in the prostate gland, occur in men over 40 YOA. Can be due to low-grade chronic prostatitis. Occurs in men >40 YOA. Overly the symphysis pubis. Patient will have a history of prostatitis. Radiographic Findings: Calcification in the prostate is often obscured by gonadal shielding. Overly the symphysis pubis. Clinical Significance: Of no or minimal significance (so dont care if obscured by gonadal shielding). Must differentiate prostate enlargement from prostate calcification by the SIZE of the prostate (prostate calcification has nothing to do with prostate cancer). Often asympatomatic and do not require treatment. Typical scenario: Elderly male, calcification often obscured by gonadal shielding. Usually a history of prostatitis, and usually/often asymptomatic and do not require treatment. Note: Prostate carcinoma and BPH are no associated with calcification. Vas Deferens Calcification Causes: degenerative phenomenon, or in IDDM males. Radiographic Findings: Serpentigious calcification (snake-like). Tube like calcifications in the lower parts of the pelvic cavity. Clinical Significance: Patients are predisposed to calcifications in the vas deferens if they are type I diabetics (insulin dependent) with poorly controlled blood sugar levels. No clinical significance. Renal Cystic Calcification Sometimes cysts on the kidneys can calcify. DDx; Benign cysts Renal cell carcinoma Hydatid cysts (occur where blood filtering occurs) often referred to as echinococcal disease. Echinococcus tapeworm which may lodge in the liver, lungs or kidneys typically

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Radiographic Findings: Cystic calcification in the liver, lungs, or kidneys. Looks like a cyst with calcification surrounding. Clinical Significance: Look for hx of being exposed to infections (working around animals). Refer to an internist for surgical removal or the cyst, and prescription of antibiotics. Tx: Surgical excision/removal. Splenic Cysts 80% are pseudocysts. Causes: (blunt) trauma (M/C), infection, infarction. You wont see the calcifications in the acute phases, only the chronic phases.

Solid Mass Calcifications

Diverse features of calcification. Extensive but diverse calcification in a solid organ or tumor. Ex: mesenteric nodes, uterine fibroids, metastasis, adenoma, spleen (Sickle cell disease). Varied in shape. Irregular calcified border, which is more dense. Interrupted margins. Extensive interior calcification with scattered luscencies/flocculent calcification, etc. Mesenteric Lymph Nodes Irregular calcifcation. Mobile. DDx: Renal or ureteric calculi. Radiographic Findings: Occur in clusters. Abdomen. Clinical Significance: usually asymptomatic. Dermoid Cysts/Teratoma Binign ovarian tumor. 16-55 yoa. Bilateral up to 25%. Arise from one pleuripotential cell. Bizarre because they have many types of Mcells. May form hair, teeth, cartilage. Risk of twisting/rupture. Clinical Significance: May or may not be symptomatic. If they are symptomatic, they may have abdominal and/or low back pain, mass, abnormal uterine bleeding, urinary frequency. These patients need to have US done. Refer to OBGYN. Uterine Fibroid/Leiomyoma M/C pelvic tumor. Women > 30 YOA to menopause. Radiographic Findings: Large, seems to form one solid mass/clump of calcification. Will have irregular borders and the internal calcifications will look irregular.

Hydatid Cysts Cysts due to parasitic infection getting lodged in the liver, lungs or kidney (zoonosis). They occur in the larval cysts stage of the tapeworms Echinococcus granulosus, so its

RADIOLOGY REVIEW
Clinical Significance: Symptoms: abdominal fullness, gas or constipation, bleeding between periods or heavy menstrual bleeding, increased urinary frequency. Refer to OBGYN. Refer them for diagnostic US. Tx: depends on the pts age, symptoms and desire for children in the future. Condiut Wall Calcifications Wall of channel or vessel for fluids becomes calcified. Think arterial, but can also calficy other channels. Ex: urinary tract, pancreatic ducts, vas deferens, fallopian tubes, biliary ducts and blood vessels. Most commonly in arties such as the abdominal aorta, but can also occur in other tubes. Radiographic Findings: Parallel, linear opacities or ring-like. Border may be indistinct, discontinuous, irregular margins. No internal appearance (no calcification on the internal part of the vessel, just in the surrounding tissue). Vary in appearance from specks to parallel and branching tracks (ring like when seen en face). Most common in the aorta and iliac arteries. In patients >40 yoa. Atherosclerosis, smoking, diabetes, hypertension. They should be PARALLEL. Clinical Significance: Diagnostic US to screen/dx. CT angiography can measure the size and extend of the aneurysm. If you see aneurysms, they need referral immediately. This is an emergency. Send them to the hospital/Emergency room. Only if the patient is in dire need, do you call 911. Note: Just because the patient doesnt have calcification in their artieries, doesnt mean that s/he doesnt have atherosclerosis. They just dont have enough calcium build up to show up on the radiograph. If theres calcification and not aneurysm present lok to see if the pt has risk factors for aneurysms (signs of atherosclerosis, no medical management for this condition). If theyre already being managed, just monitor them and make sure that the signs dont progress to aneurysm. Do a complete vascular assessment. Splenic Artery Calcification Radiographic Findings: RUQ snake like calcification between the lower ribs. You might see ring like calcifications as well. (Tortuous course). Serpent like calcification in RUQ. Note: As long as there is no dilation of the artery and the walls of the spleen are fine, then this is of no significance. Make sure to differentiate this from calcificatios in the spleen, because management is different. Vas Deferens Non inflammatory cuases in bilateral. M/C related to diabetes mellitus. May also relate to aging. Unilateral and irregular pattern suggests chronic inflammation such as TB infection Radiographic Findings: Serpentine calcification. Fallopian Tubes Can be seen following TB infection. DDx: lymph nodes and phleboliths. Radiographic Findings: May appear tube-like or rounded. Diverticular Densities When a person has a barium study done, the barium gets trapped in the diverticula (outpouching) of the colon. In some cases, the barium gets trapped in the appendix. Radiographic Findings: The densities look like chocolate chips (!!!!). Clinical Significance: often in an older individual. Calcification of Abdominal Tumors Malignant tumors of the kidney, liver, ovary and pancreas (at least) can have calcification.

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Clinical Significance: The presence of calcification in an abdominal mass or tumor is not a prediction of benign or malignancy.

Differential Diagnoses Lists for Abdomen

Hepatomegaly Fatty Liver (alcoholism, cirrhosis) Malignancy (hepatoma, metastasis (M/C)) Lymphoma CHF Hepatitis Hemolytic anemias Metabolic storage diseases Osteopetrosis Pringles Causes in lab: Anemia Leukemia Lymphoma Tumor Infection (not trauma).

Splenomegaly Lymphomas*

 Leukemias* Anemias* Mononucleosis Parasitic infections Cirrhosis Or Pringles causes in lab: Anemia Leukemia Lymphoma Tumor Infection Trauma The acronym for this one is ALL TIT (haha) Trauma* (this is a clue to look for fractures) Causes of Calcified Lymph Nodes Prior infection (TB or Histoplasmosis)

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Causes of Calcific Foci in the Liver and Spleen Previous widely dissemination infection: TB, Histoplasmosi, Brucellosis, fungal infections, and hemangioma (if in spleen only).

Adrenal Calcifications Old TB Addisons (1/3 of pts) Birth Hemorrhage Idiopathic

Unilateral Kidney Enlargement Congenital hyperplasia (usually associated w/ hypoplastic opposite kidney) Agenesis of one kidney (rare) Obstructive hydronephrosis* Polycystic disease (usually bilateral) Neoplasm* (Wilms Tumor, Renal Cell Carcinoma, Metastasis)

Pancreatic Calcifications Chronic pancreatitis Alcohol abuse (#1 reason) Diabetes mellitus (#2 reason) HPTH Pancreatic tumors (rare)

Bilateral Kidney Enlargement Acute glomerulonephritis* Lymphomas/Leukemias* Polycystic disease* Others

Nephrolithiasis/Kidney Stones (stones in the renal pelvis) HPTH* Multiple Myeloma* Lytic Mets* Leukemia Gout Tums/Coffee Genetics

Abnormal Small Bowel Air Small bowel obstruction* Adynamic ileus* Aerophagia

Common Causes of SBO Adhesions* (from previous abdominal sx) Tumors

Causes of Nephrocalcinosis (stones in the parenchyma of the kidney from increased serum calcium) HPTH Hypervitaminosis D Cancer w/ bone mets (bone is being destroyed and Calcium is being transferred into the blood). Sarcoidosis (the great mimic)

Common Causes of Adynamic Ileus Surgery* (bowel stops for 3-4 days) Infections* (appendicitis, cholecystitis, pancreatitis)

RADIOLOGY REVIEW
MM DDx list for laminated lucencies in the bladder Bladder Stones Supplements the pt is taking Suppositories

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*Note if you see a few calcifications together that dont fit into ANY organ or structure, then your default should be calcified lymph nodes. Look for a history of prior history of infection.

Vas Deferens Calcification LBO Colon carcinoma** Diverticulitis** Cecal volvulus Peritoneal metastases Massively distended bladder or other pelvic mass Adhesions Degeneration Poorly controlled blood sugar levels in IDDM (Type I DM)

The End.

Pneumoperitoneum/Extraluminal Air Recent laparotomy (lasts 3-7 days) Trauma (iatrogenic or severe external forces) Perforated abdominal viscus (gastric or duodenal ulcers) Other causes include abscesses (subphrenic and other), biliary fistula, cholangitis, pneumatosis coli, nectrotising enterocolitis or portal pyaemia.

Causes of Ascites Cirrhosis Pancreatitis Chronic renal failure And others

Air in the Biliary Tree Surgery Stone ruptured into small bowel Malignant Tumor