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Dx. Imaging Final Review

Principles of X-ray interpretation . Outside in thinking"7 categories of bone disease (CATBITES)Congenitalinclude localized and generalized skeletal anomaliesLocalized anomalies include segmentation defects in the spine (block vertebrae, hemivertebrae), pelvic vaults (congenital hip dysplasia)

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Dx. Imaging Final Review

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    1. Dx. Imaging Final Review

    2. Principles of X-ray interpretation Outside in thinking 7 categories of bone disease (CATBITES) Congenital include localized and generalized skeletal anomalies Localized anomalies include segmentation defects in the spine (block vertebrae, hemivertebrae), pelvic vaults (congenital hip dysplasia), and limb variations Arthritis Trauma Blood (Hematologic) Infection Tumor Endocrine, Nutritional, Metabolic Soft Tissue (extra)

    3. Predictor Variables Analysis of the lesion Skeletal location Position within bone Site of origin could be soft tissue that broke into bone, like infectious agents metastasis ? spreading to bone Shape the more round the more aggressive, and if it is round and effects cortex its BIG trouble Size Margination What is the edge of the bone like? If you can see an outline between good and bad bone then it is a slow infection or tumor.

    4. Cortical integrity a benign process cannot break cortex, an aggressive can Behavior of the lesion Matrix Periosteal response Normal bone you CANNOT pick out periosteum but when you do see it, then it is bad. Soft tissue changes look for tumor or periosteum changes Joint changes If tumor there should be NO joint involvement

    5. Preliminary Analysis Clinical data age Sex some infections can be gender biasis race history most important Number of lesions Symmetry of lesions Systems involved review of symptoms

    6. Dysplasia By definition: skeletal dysplasia are the result of faulty development Many are known to be the result of specific genetic mutations and are inherited. Many are congenital; fewer develop in adolescence or early adulthood many are discovered at BIRTH = congenital

    7. Achondroplasia Most common congenital dwarfism, is an autosomal dominant disturbance in epiphyseal chondroblastic growth and maturation Achondroplasia aka chondrodystrophia fetalis aka chondrodystrophic dwarfism aka micromelia Pelvic inlet in dwarfism is very small in width and the inferior pubic ramus is also very short in width Enchondral bone growth at the physis is the most common bone growth effected by achondroplasia Abnormal femur neck angle could be above 130 or below mostly genu varum

    8. Achondroplasia The pelvic bone of achondroplasia is more squared off and also the scapula is more squared off In the adult achondroplasia we get canal stenosis in the lumbar spine because we see on x-ray the pedicles get closer together, most common cause of paraplegia. In normal long bones in achondroplasia we see the width of bones is normal but we see there short length especially in proximal bones. (Rhizomelia) Effects upper extremity the most Posterior Scalloping of lumbar bodies from CSF pulsations dural ectasia (looks like a concave portion of post. body) Bullet nose vertebra appear in patients with achondroplasia Most common cause of lethal dwarfism is a small foramen magnum

    9. Achondroplasia Brachycephaly = short skull anterior to posterior Depressed nasal ridge Protruding abdomen because of hyperlordosis and prominent buttock because of pelvic structure Elbow joint has problem flexing Trident hand = when they open there hand, thumb is by itself, 2nd & 3rd finger is by itself and 4th and 5th are by itself Champagne glass appearance of the pelvis. Mass of cartilage is increased making disc as tall as vertebral body

    10. Cleidocranial dysplasia Skull and clavicular anomalies, as well as midline defects spina-bifida occulta interrupted SP development cleft palate or high arch may not have a symphysis pubis Maxilla is small, but the mandible is big Another element is funnel chest Caused by a mutation of chromosome 6 and is characterized by faulty ossification of the intramembranous and enchondral bones Skull does not interdigitate on the suture it is a lot of wormian bone, gives a hot cross bun appearance. Brachycephaly, widened intraparietal diameter

    11. Marfans Syndrome Have problems with connective tissue Heart valves, walls pathology, also lens dislocation in the eyes, long, slender bones, ocular abnormalities, and aortic aneurysm. Has congenital contractural arachnodactyly or dolichostenomelia Have extremely big feet like ~ size 15, and hands which is called (arachnodactyly) Skull reveals dolichocephaly (a long ventrodorsal head, short width, the parietal suture doesnt allow growth) - Have more ligamentous laxity than the average person so they are considered hypermobile - Thumb sign: fold thumb across hand and make a fist and you look for the thumb to stick outside the medial side of the hand, someone with Marfans can stick out till there distal phalanx is exposed

    12. Marfans (contd) Scoliosis is typical with marfans syndrome 80% of marfans will have ocular problems of lens dislocations Thoracic cage abnormality: pectus excavatum which is a depressed sternum (characteristic of Marfans) pectus carinatum - Pengium chest the whole sternum is very pronounced. (this is not tied to Marfans) Posterior Scalloping of spinal vertebra (Dural Ectasia) neurofibromatous, achondroplasia, TB of the spine, a few more (not a sign of Marfans)

    13. Hurlers Syndrome Represents the classical prototype of mucopolysaccharide disorder Aka: gargoylism, osteochondrodystrophy Individuals become dwarfs Hepatosplenomegaly is characteristic Hands are trident sometimes clawed Ribs are widened anteriorly (paddle look)

    14. Important Points on BBDs In Brittle Bone Diseases most die prematurely or at birth or as an infant. Have excessive dental caries

    15. Brittle Bone Diseases Aka Sclerotic Bone Disease Dr. Kuhn thinks of lists, like have a pathology eliminate diseases Meta-diaphyseal region is the most likely region of Osteogenesis Imperfecta (OI) Normally there is a 50/50 ratio between cortical bone vs. trabecular bone Exuberant callus formation after a bone fracture Calluss are HUGE Most OI people are not that tall on average 3 feet tall, this is for the most severe cases The 4 major clinical criteria: Osteoporosis with abnormal fragility of skeleton Blue sclerae Abnormal dentition Premature otosclerosis

    16. Osteopetrosis (Brittle Bone Disease) Effects young people like single digit kids They dont get the phases of fetal bone, to adolescent bone, to adult bone. It keeps the fetal bone and builds this is what makes the density so high Osteopetrosis Chalk Bone, bone is very dense Sclerosing Dysplasia and Brittle Bone Disease Hallmark = anemia In a KID bone marrow is red Anemia is always a part of this patients life normocytic anemia

    17. Osteopetrosis (contd) If osteopetrosis congenitalia anemia is often fatal Ruggered Jersey sign or (sandwich vertebra) is a way to tell osteopetrosis in the spine because the vertebra look like sandwiches. The vertebra are like this because of hyperparathyroidism growth plate which is the ring apophysis Osteopetrosis Tarta The level of bone they have determines the level of anemia they have Osteopetrosis tarta is sometimes diagnosed after birth or sometimes decades after The worst is osteopetrosis congenital is most severe Plain film vs. MRI for sandwich vertebra on MR is reversed compared to plain film Osteoblastic Metastasis is aka Metts Osteopetrosis also has endobones which produces a bone within a bone appearance The ilium demonstrates multiple, dense curved lines paralleling the iliac crest. Looks like little circles in the crests

    18. OI tarda these people are diagnosed after birth, which is a late diagnosis OI congenitalia is diagnosed either at birth or before birth OI is congenital and hereditary Undertubulazition long hands but the width is very small When we get premature maturazation is when the growth plate closes to quickly and the bone doesnt strengthen Short digits are brachydactalyly They are missing the connective tissue which helps structure the crystal lattice for bone

    19. Pyknodisostosis (Brittle Bone Disease) Looks a lot like the Kiebler elf Characterized by: Increased bone density Dwarfism Skeletal fragility Skeletally immature Face is small but the cranium is huge Acroosteolysis Hypoplasia or absence of the lateral ends of the clavicles and terminal tufts of the fingers and toes is a consistent finding of pyknodisostosis Stays close to the lateral and medial phalanx Bowing and overgrowth of the radius (Madelungs Deformity)

    20. Sclerosing Dysplasia Melorheostosis Has to much bone laid down both on the inside of the bone and on the outside Is not a brittle bone disease Dripping wax appearance is a common finding in Mellory the flowing nature Another form is when we fill in the proximal and distal end of the long bone with extra bone Most common complaint is pain by putting pressure on arteries, veins, and nerves. Leading to lymphedema, vascular occlusion, or bursal inflammation

    21. Osteopoikilosis Its hallmark is spotty bone periarticular spots Islands of cortical bone Patient is asymptomatic Looking for a benign history Its a sclerosing dysplasia If the patient is 25 y/o then label Osteopoikilosis and then forget it, if a 55 y/o probably Osteopoikilosis but could be osteoblastic metastasis

    22. Aperts Disease - Abnormal separation of hand joints called Mitton Hand Depressed cerebration aka cognitive disabilities Brachycephaly short skull We see this when the coronal suture fuses to early, so head is longer A-P Scaphocephaly Is when the mid-sagittal suture closes to early and the height of the skull will be short

    23. Tricorhinophalangeal Distal phalanx is very small Rhino = nose thin but bulb nose (think of Harry Potter head elfs nose) Very fine hair = trico (course) And short in stature

    24. Chondrodysplasia punctata Stippledepiphysis Multiple growth centers If we note strippled epiphysis we try and keep them away from sports that are high in impact to keep there bones growing normally A bunch of dots on bones in kids

    25. Spondyloepiphyseal dysplasia Hallmark is in the spine have a convexity on the top and bottom of the vertebra to where a normal vertebra has a concavity It is humped up because of fewer rings around the body of the vertebra it is not more bone. Less bone around the growth ring of the apophysis

    26. Progressive Diaphyseal Dysplasia (Caffeys Disease) Looks a lot like Melorheostosis but only has wavy excess of bone in the diaphysis

    27. Layers of the Skull Outer and inner are cortex Middle is diploic layer (space) Hyperostosis Hyperostosis frontalis internis is an outgrowth of bone in the frontal lobe They have no diploic space No clinical significance, but does not effect brain function Parietal foramen Clinical significance: Yes, but not serious, because the dura is very tough Normally bilateral

    28. Contd Failure of Segmentation (AKA Block Vertebra) Embryological failure of scleratome segmentation and separation 1st described by Macalister in 1883 (Roentgen made first x-ray in 1902) Ways to have blocked vertebra Congenital Premature DJD Wasp waist appearance Rudimentary disc (a not well developed disc) Acquired Ankylosing spondylitis Osteomyelitis Surgery Infection

    29. Cranial vertebral synostosis Cranium and C1 are fused It has an analomous foramen COC1 block which has a major problem with instability which has a traumatic effect on the cord Most serious complication of a blocked vertebra The C1 SP and occiput makes a anomalous foramen and you will see it on the LATERAL

    30. Congenital and Acquired are the 2 typical cases Congenital Blocked Vertebra On an oblique view the middle of the blocked vertebra will be the thinnest bringing on a Wasp Waste Appearance Rudimentary Disc is what is left on a blocked vertebra, shows up as a little black dot Congenital blocked vertebra will be fused both on the anterior and posterior aspect including the facet joints Most common complication is premature DJD The object we always look at during a flexion is the ADI and that is very important to look at in a blocked vertebra

    31. Soft Tissue Calcification Defined by level of Serum of Ca++ and the tissue Cartilage is the 2nd most likely object that will take up bone, its only beat by pre-bone Physiologic normal serum and normal tissue uptake Dystrophic serum Ca levels are normal but the tissue is abnormal Tendonitis, bursaitis, etc. Metastatic primary process that has a distant progression Elevated Ca + with normal tissue Ex: Hyperparathyroidism

    32. Posterior Ponticle another example of physiologic S.T. Calcification aka Arcuate foramen 15% of the population has this Approx 10% of the patients with arcuate foramen demonstrate signs and symptoms most of the time vertebral aa compromise Know the difference of Arcuate foramen and anomalous foramen

    33. Os odontoidium Odontoid Process not connected to the C2 vertebra called Os odontoidium Clinical Sig.: Too much translation (A?P) Os odontoidium the dens does not ossify to the body of C2, so leaves a problem with translation, very big in KF syndrome Overall considered uncommon Ununited ossification centers Long standing non-union fracture trauma Need to do an MR study to rule in or out

    34. Blocked Vertebra Will be able to see IVFs on a neutral lateral view, instead of a typical oblique film One big worry of blocked vertebra is its effect on the ADI Spinolaminar line is not correct in a blocked vertebra The first result most of the time with blocked vertebra is DJD

    35. Contd Distinguish between congenital vs. acquired LOOK FOR THE SCAR on the neck Rule: when you see one anomaly, look for another. Wasp waste is congenital Posterior elements are fused together = congenital

    36. Contd Multiple Blocked vertebra = Klipple Feil syndrome unilateral high scapula Sprangles deformity oma vertebral bone vertebra to vertebra bone bar Pectis excavatum the heart is being squashed Measure thoracic A-P from T8 to back of sternum should be roughly 10cm Listening to heart for murmurs we listen for pathologies this could be indicative to Straight Back Syndrome

    37. Pterygium Coli when there clavicle and shoulder are not moving (scalenes)

    38. Agenesis of Anterior and Posterior tubercles of C1 (spina bifida)(spondyloschesis book terminology)

    39. Sprangles Deformity elevation of the scapula and clavicle, which has NEVER been in the right spot and was a failure to descend. Usually unilateral

    40. Downs Syndrome (trisomy 21) Recognizable at birth Brachycephaly (A-P) Small nose w/ a flat bridge Slanting eyes Protruding eyes Protruding tongue Depressed cerebration a constant

    41. D.Syndrome Contd X-ray film huge ADI Small spinal canal = small space for spinal canal If you have an intrusion in the spinal canal on an MRI 20% of all downs have absence of the transverse ligament so they shouldnt be allowed to tuck chin to chess thats dangerous stress views pre-participation exam do free exams for those special individuals Leukemia much more common in Downs

    42. Multiple Hemi Vertebra Should go level by level vertebra Aka Scramble Spine Spine is going up on wedged vertebrae

    43. Costal Chondral calcification Physiologic calcification of costal cartilage

    44. C1 TPs are suppose to be pretty lateral, if C1s TPs are angled downward they is really no clinical significance. Spina Bifida Occulta Not clinically significant Ununited Growth Center Looks like a fracture but it is not Its just congenital anomaly Not clinically significant The outside will be a solid white line (cortical bone is in tact)

    45. If a patient has physiological calcification in a tissue the Ca levels in the body is normal If it is high than it is metastatic Bilateral Overhang Sign Is a burst fracture of C1 For every symptom or clinical finding look at the mechanism of injury to see if it fits.

    46. Pectics Excavatum Clinically significant Have to worry about straight back syndrome Worries of murmurs are normally present but they are benign Very high arched appearance of the posterior ribs <10 cm front of body of vertebra to sternum can cause pathologic heart murmurs Another form Pectics Karanatum

    47. G.O.K. (God only knows) Most likely just a congenital anomaly. Something that just cant be explained how or when it happened except most likely had it from birth.

    48. Limbus Vertebra No clinical significance, except could be mistaken for bone fracture Apparently happens when patient is young enough to make up bone, the nucleus pulposus goes through the growth plate, Schmorals Node, and breaks a piece off making it an acquired normal variance This was most likely produced by axial load Below the age of 18, really likely before 15 years of age

    49. Absent Pedicle Lytic metastasis is the most likely reason for a missing pedicle The 2nd most likely reason for absence is agenesis If we have a pedicle that isnt there and the other side is we get a vertebra that has to do the work of 2. Agenesis or Hypoplasia On CT we should see trabeculae on the inside by the pedicle but if one is doing the work of 2 then we should see considerably more cortical bone

    50. Anterolisthesis Congenital absence of posterior arch, 7% of population has anterolisthess Congenital is possible but it is not what we expect to see stress fracture this is where most people fall into the category Mostly due to stress fractured of the pars interarticularis People like: Gymnasts Divers Anterior lineman of football Eskimos (Inawits) 40% found to be spondylolisthesis The Eskimos who live in town have about 7% chance

    51. Contd Facet surface degeneration Acquired trauma Pathologic could be tumor metastisis Overall look at spondylolytic vs degeneration Intersegmentally stable and unstable films The way to view this is a distracted view and view it, then have then wear a backpack and do a 2nd film If a person has 3mm different or more from distracting to loading we declare them intersegmentally unstable.

    52. Sacralization aka: Lumbarization 1A Asymmetric 1B Bilateral TPs (these 2 have big TPs) Normal disc, variation from normal, but no clinical significance

    53. 2A pseudoarticulation accessory joint is the real name that should be used, has a single accessory joint has the highest clinically significant herniated disc, as high as 80%, and the level above approaching 50% transitional disc THE WORST OF ALL 2B bilateral accessory clinically significance, close to 40% at the lower level joint and 27% on the level above it

    54. Contd 3A bone bar, uniting TP of L5 with the sacral ala No clinical significance 3B bilateral bone bar no clinically significance classic sacralized segment IV hybrid appearance bone bar on 1 side and accessory joint on the other

    55. If a patient get localized back pain, L5 SP may be jamming up against S2 tubercle or S1 whenever they extend, usually happens around 30-40 y/o normally because a change in disc height. They call this S2 hypertrophy

    56. Knife-clasp deformity Spina-bifida occulta in the sacrum when a patient extends backwards and gets a LIGHTNING strike down the back of his leg suspect that L5 is touching nerves in the sacrum through the opening. They dont have to be symptomatic either

    57. Sacral Agenesis Patient is loaded (mechanically) Sacrum is not there, did not develop L5 sits on ileum

    58. When the angle goes below 120 degrees we get Coxa Vara, if the angle is above 130 then it is Coxa Valga (rarely call it coxa valga and rarely see) most of coxa valga are immature bone

    59. Fabella Normal variant Accessory ossicles Very predictable close to 50%, common Found in lateral head of gastrocnemius Always found in lateral condyle of femur Joint Mouse torn off piece of cartilage sometimes the bodies own cleanup mechanism can take care of joint mouse hangs out in interchondrylar space/notch Can be chondral, not show up on plain film, but they calcify and then we see them on plain film Clinical significance: Patients usually have an axial load and rotational injury/trauma which will chip off cartilage making or developing a Fabella

    60. Enchondral literally means in cartilage Enchondral bone growth closes after puberty, think of Acromegaly Intramembranous is the bone type we keep for a lifetime Sesamoid Accessory bones If they divide they are called bisected-sesamoid No clinical significance If the person has more than 5 phaylanx is called polydactyl

    61. Supracondylar process (bone process) Sturthers ligament is the ligament sometimes attached to this process may lead to a neurovascular entrapment Happens in children mostly, can occur in adults No clinical significance Always comes off the distal portion of the humerus and points to the elbow Clinical significance: may break off and struthers ligament tends to entrap ulnar nerve Osteochondroma Made of bone and cartilage Can occur in any location if it happens on the humerus it will point away from the elbow, no ligament attached, no smooth outer layer, ends can appear as an aggressive process

    62. Synostosis blocked vertebra in the hand A failure to unfuse or separate, commonly B/L (not always) Any of joints can fuse

    63. Cupids Bow Notocortical Persistency Patients have nucleus pulposus divided into 2 concavities Arch in the vertebral endplate, normally happens in lumbars but can occur higher

    64. Hypoplasia Hypoplasia of a shallow acetabulum Center edge angle is lowered or raised Osteomalacia is increased angle 2nd DJD of hip joint Focal Hypoplasia (hemiplasia of hip) Hypoplasia is just a diminished growth of bone

    65. Rocker bottom of foot Not a big talus, or navicular, or cuneiforms, or cuboid Soft tissue is very stretched Abnormal development

    66. Accessory ossicles and calcific tendonitis are the two possible pathologies if you see density in the foot If you stretch the tendon it will hurt If it doesnt hurt on palpation then it is accessory ossicles

    67. Bayonet wrist When the ulna is totally displaced sticking out like a bayonet Madelung wrist (the carpals and ulna and radius are totally lumped together)

    68. Ulna minus No treatment, but increased incidence of lunate subluxation and Scaphoid fracture (NBQ) Basically a short ulna

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