Back Clinic Imaging & Diagnostics Team. Dr. Alex Jimenez works with top-rated diagnosticians and imaging specialists. In our association, imaging specialists provide fast, courteous, and top-quality results. In collaboration with our offices, we provide the quality of service our patients’ mandate and deserve. Diagnostic Outpatient Imaging (DOI) is a state-of-the-art Radiology center in El Paso, TX. It is the only center of its kind in El Paso, owned and operated by a Radiologist.
This means when you come to DOI for a radiologic exam, every detail, from the design of the rooms, the choice of the equipment, the hand-picked technologists, and the software which runs the office, is carefully chosen or designed by the Radiologist and not by an accountant. Our market niche is one center of excellence. Our values related to patient care are: We believe in treating patients the way we would treat our family and we will do our best to ensure that you have a good experience at our clinic.
SKULL FX: COMMON IN THE SETTINGS OF HEAD INJURIES. SKULL FX OFTEN POINT TO OTHER COMPLICATING FACTORS: INTRA-CRANIALHEMORRHAGING, CLOSED TRAUMATIC BRAIN INJURY AND OTHER SERIOUS COMPLICATIONS
SKULL X-RAYS ARE VIRTUALLY OBSOLETE IN EVALUATING HEAD INJURY. CT SCANNING W/O CONTRAST IS THE MOST IMPORTANT INITIAL STEP IN EVALUATION OF ACUTE HEAD TRAUMA. MRI HASA POOR ABILITY TO REVEAL SKULL FRACTURES, AND NOT TYPICALLY USED FOR AN INITIAL DX OF ACUTE HEAD TRAUMA.
SKULL FX ARE IDENTIFIED AS FXS OF SKULL VAULT, SKULL BASE AND FACIAL SKELETON EACH ASSOCIATED WITH SPECIFIC FEATURES AND HELP TO PREDICT COMPLICATIONS.
LINEAR SKULL FX: SKULL VAULT. M/C FX. CT SCANNING IS THE KEY TO EVALUATE ARTERIALEXTRADURAL HEMORRHAGING
X-RAY DDX: SUTURES VS. LINEAR SKULL FX. FX IS THINNER, �BLACKER� I.E. MORE LUCENT, CROSSESSUTURES,�AND VASCULAR GROOVES, LACKSSERRATIONS
RX: IF NO INTRACRANIAL BLEEDS THAT NO TREATMENT. NEUROSURGICAL CARE IF BLEEDSDETECTED BY CT SCANNING
DEPRESSED SKULL FX: 75% IN THE VAULT. CAN BE DEADLY. CONSIDERED AN OPEN FX. MOST CASES NEED NEUROSURGICALEXPLORATION ESPECIALLY IFFRAGMENTS DEPRESSED >1-CM.COMPLICATIONS: VASCULAR INJURY/HEMATOMAS, PNEUMOCEPHALUS, MENINGITIS, TBI, CSF LEAK, BRAIN HERNIATION ETC.
IMAGING: CT SCANNING W/O CONTRAST
BASILAR SKULL FX: CAN BE DEADLY. OFTEN ALONG OTHER MAJOR HEAD TRAUMA OF THE VAULT AND FACIALSKELETON, OFTEN WITH TBI AND MAJORINTRACRANIAL HEMORRHAGING. OFTEN OCCUR AS �HEADBAND� EFFECT OF IMPACT AND MECHANICAL TENSION THROUGH THE OCCIPUT AND TEMPORAL BONES THROUGH SPHENOID AND OTHER BASE OF SKULL BONES. CLINICALLY: RACCOON EYES, BATTEL SIGN, CSFRHINO/OTORRHEA.
Facial Fractures
NASAL BONES FX: 45% OF ALLFACEFXM/C IMPACT IS LATERAL(FIST BLOW ETC.) IF UNDISPLACEDNO TREATMENT, IF DISPLACED MAY COMPLICATE AIR FLOW AND RESPIRATORY PASSAGE, MAY BE ASSOCIATED WITH OTHER FACIAL/SKULL INJURY. X-RAYS 80%SENSITIVE, FOLLOWED BY CT INCOMPLEX INJURIES.
ORBITAL BLOW OUT FX: COMMONORBITAL INJURY D/T IMPACT ON THE GLOBE AND/OR ORBITAL BONE. FX OF ORBITAL FLOOR INTOMAXILLARY SINUS VS. MEDIAL WALL INTO ETHMOID SINUS. COMPLICATIONS: ENTRAPPEDINFERIOR RECTUS M, PROLAPSEORBITAL FAT,�AND SOFT TISSUES, HEMORRHAGING AND OPTIC NERVE DAMAGE. RX: CONCERNS OF GLOBE INJURY ARE IMPORTANT, GENERALLY TREATEDCONSERVATIVELY IF NO COMPLICATIONS PRESENT
TRIPOD FX: 2ND M/C FACIAL FX#AFTER NASAL (40% OF MIDFACEFX) 3-POINT FX-ZYGOMATICARCH, ORBITAL PROCESS OF ZYGOMATIC BONE & SIDE OF MAXILLARY SINUS WALL, MAXILLARY PROCESS OF ZYGOMATIC BONE.COMPLICATED BY NERVE INJURY, TEMPORALIS M DAMAGE ETC. CT SCANNING IS MORE INFORMATIVE THAT X-RAYS (WATER�S VIEW).
LEFORT FX: SERIOUS FX ALWAYS INVOLVES PTERYGOID PLATES, POTENTIALLY SEPARATINGMIDFACE AND ALVEOLAR PROCESS WITH TEETH FROM THE SKULL. CONCERNS: AIRWAYS, HEMOSTASIS, NERVE INJURIES. CT SCANNING IS REQUIRED. POTENTIAL RISK OF BASILAR SKULL FX
PING-PONG FX:�EXCLUSIVELY IN INFANTS. AN INCOMPLETE FX D/T FOCALDEPRESSION: FORCEPS DELIVERY, DIFFICULT LABOUR ETC. FOCALTRABECULAR MICROFRACTURIINGLEAVING DEPRESSION RESEMBLING APING-PONG. DX IS MAINLY CLINICALSEEN AS FOCAL DEFECT �DEPRESSION� IN THE SKULL. TYPICALLYNEUROLOGICALLY INTACT. CT MAY HELP IF BRAIN INJURY IS SUSPECTED. RX: OBSERVATIONAL VS. SURGICAL IN COMPLICATED INJURIES. SPONTANEOUSREMODELING HAS BEEN REPORTED
LEPTOMENINGEAL CYST (GROWING SKULL FX)- ARE AN ENLARGING SKULL FRACTURE THAT DEVELOPS ADJACENT TO POSTTRAUMATIC ENCEPHALOMALACIA
IT IS NOT A CYST, BUT AN EXTENSION OF THEENCEPHALOMALACIA THAT SEEN A FEW MONTHS POST-TRAUMA WITH PREVIOUS SKULL FX FOLLOWEDBY HERNIATION OF THE MENINGES AND ADJACENTBRAIN WITH PULSATIONS OF THE CSF. CT IS BEST ATDX THIS PATHOLOGY. INDICATES: GROWING FX AND ADJACENT ENCEPHALOMALACIA AS FOCALHYPOATTENUATING LESION.
DDX: INFILTRATING CELLS/METS/OTHER NEOPLASMSINTO SUTURES, EG, INFECTION ETC.
MANDIBULAR FXS: COMMON. POTENTIALLYCONSIDERED AN OPEN FX D/T INTRA-ORALEXTENSION. 40% FOCAL BREAK DESPITEMANDIBLE BEING A RING. DIRECT IMPACT(ASSAULT) M/C MECHANISM
PATHOLOGICAL FX D/T BONE NEOPLASMS, INFECTION ETC. IATROGENIC DURING ORAL SURGERY (TOOTH EXTRACTION)
IMAGING: MANDIBLE X-RAYS, PANOREX, CT SCANNING ESP. IN CASES OF ASSOCIATEDFACE/HEAD TRAUMA
COMPLICATIONS: AIRWAY OBSTRUCTION, HEMOSTASIS IS A MAJOR CONSIDERATION, DAMAGE TO MANDIBULAR N, OSTEOMYELITIS/CELLULITIS AND POTENTIAL SPREAD THROUGH FLOOR OF THE MOUTH (LUDWIGANGINA) AND NECK FASCIAL SOFT TISSUES INTOMEDIASTINUM. CANNOT BE NEGLECTED D/T HIGH MORTALITY RATES.
RX: CONSERVATIVE VS. OPERATIVE
Acute Intracranial Hemorrhage
EPI AKA EXTRADURAL: (EDH) TRAUMATIC RAPTURE OF MENINGEAL ARTERIES (MMA CLASSIC) WITH RAPIDLY FORMING HEMATOMA BETWEEN THE INNER SKULL AND OUTER DURA. CT SCANNING IS THE KEY TO DX: PRESENTS AS �LENTIFORM� I.E. BICONVEX COLLECTION OF ACUTE (HYPERDENSE) BLOOD THAT DOES NOT CROSSSUTURES AND HELPS WITH DDX OF A SUBDURAL HEMATOMA. CLINICALLY: HA, LUCID EPISODE INITIALLY AND DETERIORATING IN A FEW HOURS.COMPLICATIONS: BRAIN HERNIATION, CN PALSY. O/A GOOD PROGNOSIS IF QUICKLY EVACUATED.
SUBDURAL HEMATOMA (SDH): RAPTURE OF BRIDGINGVEINS BETWEEN INNER DURA AND THE ARACHNOID.SLOW BUT PROGRESSIVE BLEED. MAY PARTICULARLYAFFECT THE VERY YOUNG AND ELDERLY AND IN ALL AGES (MVA, FALLS ETC.) MAY DEVELOP IN �SHAKEN BABY SYNDROME�. DX MAY BE DELAYED AND WORSEN THE PROGNOSIS WITH HIGH FATALITIES. IN ELDERLY HEAD TRAUMA MAY BE MINOR OR NOT RECALLED. EARLYIMAGING WITH CT IS CRUCIAL. PRESENTS AS CRESCENTSHAPEDCOLLECTION THAT CAN CROSS SUTURES BUT STOPPED AT DURAL REFLECTIONS. DIFFERENTATTENUATION ON CT D/T DIFFERENT STAGES OF BLOODDECOMPOSITION: ACUTE, SUBACUTE,�AND CHRONIC.MAY FORM A CHRONIC COLLECTION-CYSTICHYGROMA. CLINICALLY: VARIABLE PRESENTATION, 45-60% PRESENT WITH SEVERELY DEPRESSED CNS STATUS, PUPILLARY INEQUALITY. OFTEN WITH INITIAL BRAIN CONTUSION, THEN A LUCID EPISODE BEFORE SEVERELYDETERIORATING. IN 30% CASES OF FATAL BRAIN INJURY PATIENTS HAD SDH. RX: URGENT NEUROSURGICAL.
SUBARACHNOID HEMORRHAGE (SAH): BLOOD IN THE SUB-ARACHNOID SPACE AS THE RESULT OF TRAUMATIC OR NON-TRAUMATIC ETIOLOGY: BERRY ANEURYSMS AROUND CIRCLE OF WILLIS.SAH 3% OF STROKES, 5% OF FETAL STROKES.CLINICALLY: PRESENTS AS A �THUNDERCLAP HEADACHE� DESCRIBED AS A �WORST HA INLIFE�. PT COLLAPSES MAY OR MAY NOT REGAIN CONSCIOUSNESS. PATHOGY: DIFFUSE BLOOD INSA SPACE 1)SUPRASELLAR CISTERN WITH DIFFUSE PERIPHERAL EXTENSION, 2)�PERIMESENCEPHALIC, 3) BASAL CISTERNS. BLOOD LEAKED INTO SA SPACE UNDERARTERIAL PRESSURE INDUCES GLOBAL INCREASE IN INTRACRANIAL PRESSURE, ACUTE GLOBAL ISCHEMIA WORSENED BY VASOSPASM AND OTHER CHANGES.
DX: IMAGING: URGENT CT SCANNING W/O CONTRAST, CT ANGIOGRAPHY MAY HELP TO RULE OUT 99% OF SAH. LUMBAR PUNCTUREMAY HELP IN DELAYED PRESENTATION. AFTER INITIAL DX: MR ANGIOGRAPHY HELPS TO FIND THE CAUSE AND OTHER IMPORTANT FEATURES
IMAGING FEATURES: ACUTE BLOOD IS HYPERDENSE ON CT. FOUND IN DIFFERENTCYSTERNS: PERIMESENCEPHALIC, SUPRASELLA, BASAL, VENTRICLES,
RX: INTRAVENOUS ANTIHYPERTENSIVE MEDS, OSMOTIC AGENTS (MANNITOL) TO DECREASEICP. NEUROSURGICAL CLIPPING AND OTHER APPROACHES.
CNS Neoplasms: Benign vs. Malignant
BRAIN TUMORS REPRESENT 2% OF ALL CANCERS. ONE THIRD ARE MALIGNANT, OF WHICH METASTATIC BRAIN LESIONS ARE THE MOST COMMON
CLINICALLY PRESENT WITH LOCAL CNS ABNORMALITIES, INCREASED ICP, INTRACEREBRAL BLEEDING ETC. FAMILIALSYNDROMES: VON-HIPPEL-LANDAU, TUBEROUS SCLEROSIS, TURCOT SYNDROME, NF1 & NF2 INCREASE THE RISK. IN CHILDREN: M/C ASTROCYTOMAS, EPENDYMOMAS, PNETNEOPLASMS (E.G. MEDULLOBLASTOMA) ETC. DX: BASED ON WHO CLASSIFICATION.
IMAGING IS CRUCIAL: INITIAL SYMPTOMS MAY PRESENT AS SEIZURE, ICP SIGNS HA. EVALUATED BY CT AND MRI WITH IV GADOLINIUM.
IMAGING DETERMINES: INTRA-AXIAL VS. EXTRA-AXIALNEOPLASMS. METS FROM PRIMARY BRAIN NEOPLASMS MAYO CCUR VIA CSF AND LOCAL VESSELS INVASION
NOTE AXIAL CT SLICE OF MENINGIOMA WITH AVIDCONTRAST ENHANCEMENT.
AXIAL MRI ON FLAIR PULSE SEQUENCE REVEALED EXTENSIVE NEOPLASM AND MARKED CYTOTOXIC EDEMA OF THE BRAIN PARENCHYMA CHARACTERISTIC OF GRADE IV GLIOMA (GBM) WITH VERY POOR PROGNOSIS. ABOVE FAR RIGHT IMAGE: AXIAL MRI FLAIR: BRAIN METASTASIS FROM BREAST CANCER. MELANOMA IS COMMONLY METASTASIZESTO THE BRAIN (SEE PATH SPECIMEN) MRI CAN BE DIAGNOSTIC D/T HIGH SIGNAL ON T1 AND CONTRAST ENHANCEMENT.
RX: NEUROSURGICAL, RADIATION, CHEMOTHERAPY,�IMMUNOTHERAPY TECHNIQUES ARE EMERGING
Most healthcare providers use x-rays as a diagnostic tool to treat a variety of patient complaints, including chiropractors. They can help doctors identify the source of a problem or if there is something more going on. X-rays can also help chiropractors determine the best course of action for treatment. To understand more, let’s take a closer look at what they are and how they’re used in most chiropractic offices.
What are x-rays?
An x-ray is a very vigorous form of electromagnetic radiation that is similar to radio waves, ultraviolet radiation, microwaves, or visible light that is used to view the internal composition of a person or thing. A beam is focused on a specific part of a person�s body, such as the back, it produces a digital image of the skeletal structure.
The beam passes easily through skin and other soft tissues�but is unable to pass through bone and teeth. Soft tissue that is denser, such as organs, ligaments, and muscles, will be visible�but will be captured in shades of gray. Areas like the bowel or lungs appear on the film as black.
The use of chiropractic x-rays
Chiropractic x-rays provide vital information that can affect how the chiropractor chooses to treat a patient. In some cases, chiropractic care or spinal manipulation may not be an appropriate course of action at that time, and the patient may be started on a different, gentler therapy.
Other times, it can show the chiropractor how to best proceed in treating the patient. In short, patients can receive better, more well-rounded care which can better facilitate their healing and pain management.
Identify a condition or symptom, such as a spinal tumor or lesion�that would provide a medical reason that a specific course of care should not be done.
Obtain important biomechanical information that can aid in guiding treatment.
To stay apprised and maintain a record of a patient�s degenerative process.
Aid in identifying anomalies in the spine and joints that can affect treatment.
Allows patients to understand their condition and treatment plan better, allowing them to take ownership of the process and be more involved in their therapy and healing.
What does a chiropractor look for on an x-ray film?
When a chiropractor takes an x-ray of a patient, they are looking for things in several particular areas. The first thing they check is to make sure that there are no dislocations, fractures, cancer, infections, tumors, or other potentially dangerous conditions.
They then look for disk height and other signs of disk degeneration, bone density, bone spurs, joint spaces, and alignment. This allows them to identify conditions like scoliosis and other conditions that may require specific forms of treatment.
Many chiropractors prefer that the patient is in a weight-bearing position when taking spinal x-rays. This differs from the majority of medical facilities which have the patient lie down.
The advantage of weight-bearing x-rays as a diagnostic tool�is that it allows for measuring, i.e., leg length deficiency, scoliosis, and the narrowing of joint space. It can also show that certain bones, such as the tibia and fibula, are separating which can be an indication of a torn tendon or problem with the joint. A non-weight bearing x-ray cannot provide the same perspective,�and vital clues to a patient�s condition may be missed.
In all cases, Orthopedic hand surgical referral is required
Colles fx: m/c d/t FOOSH+pronation. m/c inOSP/elder women. Rare in men and if occurs need DEXA to avoid hip Fx etc. Young pts: high-energy trauma. Typically extra-articular.50%-cases show Ulna styloid (US) Fx.
Imaging: x-rad is sufficient, CT in complex Fx, MRI helps with ligament tears and TFC.
Rx: if extra-articular and <5-mm distal radius shortening and <5-degree dorsal angulation closed reduction+casting is sufficient. ORIF in complex cases.
�Image Dx: distal rad impaction/shortening,dorsal angulation of distal fragment, carefully examine if intra-articular extension, 50% US Fx
Smith Fx: Goyrand in French literature. Considered as reversed Colles, otherwise almost identical, I.e., 85% extra-articular, 50%US Fx, OSP/elderly women, young pts-high-energy trauma. Differences: mechanismFOOSHwith flexed wrist thus m. Less frequent.
Imaging steps: (see Colles Fx) C
Complications: similar to Colles Fx
Rad Dx: 85% extra-articular with volar(anterior) angulation of the distal fragment,radial shortening. Carefully examine cortical breach suspecting intra-articular extension that can be named as Smith type 2 or Reversed Barton Fx (next)
Rx: similar approach as in Colles.
Barton fx: FOOSH, impaction of distal radius similar to Colles but the Fx line extends from the dorsal radial aspect into radiocarpal joint resulting with dorsal slip/dislocation of the carpus.
Imaging: 1st sept x-radiography often with CTto examine intra-articular Fx extension and operative planning
Rad Dx: distal radius Fx extending from dorsal into the radiocarpal joint with a variable degree of displacement, the proximal slip of the carpus
If Fx line extends from the volar aspect into the wrist joint named Reversed Barton aka Smith type 2 (above bottom image)
Complications: similar to all distal radius Fx
Rx: operative with ORIF
Chauffeur’s/backfire Fx aka Hutchinson Fx: intra-articular Fx of Radial styloid. The name derives from the time when the car had to be started with a hand crank that could backfire inducing wrist dorsiflexion and radial deviation.
Imaging: x-radiography is sufficient. CT may be helpful if Fx not readily shown by x-rays.
Rx: operative with percutaneous lagscrewin all cases d/t intra-articularnature
Die-Punch Fx: impaction Fx by the Lunate bone into distal articularLunate fossa of the Radius. IntraarticularFx. Derives its name from a technique to shape (impress) a hole in industrial machining “die-punch.”FOOSH injury.
Imaging: 1st step x-rays, may be equivocal d/t subtle depression of the Lunate fossa then CT scanning is most informative.
Rad Dx: impacted lunate fossa region with intra-articular Fx extension. This can present as a comminuted Fxarticular Fx of the Distal Radius.
Rx: operative d/t intra-articular Fx
Construct arcs of Gilula when evaluating carpal injuries. An Important step required to avoid missing subtle changes in carpal alignment and cortical continuity
Scaphoid bone Fx: m/c Fx carpal bone. D/tFOOSH wrist extended radially deviated. Location of Fx is most important to prognosis: Waist-m/c location (70%). May have 70-100%chance of AVN. Proximal pole Fx: 20-30% with a high risk of non-union. Distal pole-10%shows better prognosis. Distal pole Fx is m/c in children. Key clinical sign; pain in the snuffbox.
Imaging: 1st step-x-radiography but 15-20%missed d/t occult Fx. Special views required. Thus MRI is the most sensitive and specific for early occult Fx. Bone scintigraphy has98/100% specificity & sensitivity esp. 2-3 days after the onset. Key rad. Dx: Fx line if evident, displacement and obscuration of scaphoid(navicular) fat pad, examine for scapholunate dissociation. If proximal bone appears sclerotic-AVN occurred. MRI: low on T1 & high on T2/STIR/FSPD d/t bone edema, a�low signalFx line can be noted.
Rx: Spica cast should be applied if clinically suspected even w/o x-ray findings. For waistFx-cast for 3-mo for prox pole 5-mo immobilization. ORIF or percutaneous pinning with a Herbert screw.
Scapholunate Ligaments Dissociation
SNAC wrist: scaphoid non-union advanced collapse. Often d/t non-union and dissociation of scapholunate ligaments (SLL)with progressive radiocarpal and intercarpalDJD. The Proximal scaphoid fragment is attached to Lunate with distal dissociating and rotating�signet ring� sign on x-rays.
SNAC wrist may often result in DISI
Rx: progressive DJD may lead to four-corner arthrodesis
Scapholunate advanced collapse (SLAC wrist): SLLdissociation with progressive intercarpal and radiocarpal DJD and volar or dorsal carpal displacement (DISI & VISI). Causes: trauma, CPPD, DJD, Kienboch disease (AVN of Lunate), Preiserdisease (AVN of Scaphoid).
SLL dissociation will lead to Dorsal or VolarIntercarlate aka Intercarpal Segmental Instability (DISIor VISI).
Rad Dx: Dx underlying cause. X-rays demonstrate dorsal or volar angulation of the Lunate with increased or decreased scapholunate angle on the lateral view. On frontal view: Terry Thomas sign or widening of scapholunate distance 3-4-mm as the upper limit of normal.
�MRI may help with ligament evaluation and pre-surgical planning
Rx: often operative with late DJD. Four-corner arthrodesis
Triquetrum Fx: 2nd m/c carpal bone Fx. M/C dorsal aspect is avulsed by the�tough Dorsal radiocarpal ligament. Cause: FOOSH.
Imaging: x-radiography wrist series is sufficient. Best revealed on the lateral view as an avulsed bone fragment adjacent to the dorsum of the Triquetrum. CT may help if radiographically equivocal.
Rx: conservative care
Complications: rare, may persist as pain on the dorsum of the wrist
Hook of the Hamate Fx: m/c occurs in batting sports (cricket, baseball, hockey, impact by a golf club, etc.) 2% of carpusFx.
Imaging: x-radiography may fail to detect an Fx unless “carpal tunnel view” is used. CT may help if x-rays unrewarding.
Clinically: pain, positive pull test, weak, painful grip. Deep ulnar n. Branch may be affected within the�Guyon canal.
Rx: usually non-operative, but chronic non-union may require excision.
DDx: bipartite hamate
�Lunate vs. Perilunate dislocation: Lunate is m/c dislocated carpal bone. Overall infrequent carpal injury. However, often missed!
Occurs with FOOSH and wrist extended and ulnar deviated. Imaging: 1st step x-rays. Ifunrewarding or require more complex injury evaluation CT scanning.
Key Rad DDx: DDx Lunate from perilunate dislocation. Lunate dislocation: lunate lost its contact with distal radius �spilled teacup� on the lateral. Perilunate dislocation: Lunate maintains its contact with distal radius despite the Capitatedorsally dislocated. Lunate dislocation is additionally helped to identify a �pie sign� d/t Lunate overlapping the Capitate
Rx: emergency reduction and operative repair of torn ligaments
Metacarpal & Phalangeal Injuries
Bennett Fx: intra-articular but noncomminuted impact-type Fx of the base of 1st MC bone of the thumb. X-radiography is sufficient.
Rad Dx: characteristic triangular fragment of bone on the ulnar aspect of the 1st MCbase, often with radial subluxation of the remaining radial aspect of the 1st MC
Complications: DJD, non-union, etc.
Rx: prone to instability/non-union requiring an operative care
Rolando Fx: aka comminuted Bennett with Y or T-configuration. More complex injury. It is unstable requiring operative care
Gamekeeper thumb: traditionally described as a chronic tear of the�ulnar (medial) collateral ligament at 1stMCP in English Gamekeepers’ who performed neck twisting/killing of small game. An acute injury may also be named as Skier’s thumb. This injury can be ligamentous w/o a fracture and an avulsion injury at the 1st proximal phalanx base.
Complication: Stener lesion or displacement of torn ligament over Adductor pollicis muscle that cannot heal w/o surgical repair. MRI Dx is required.
Avoid thumb stress views that can induce a Stenerlesion
Imaging: x-radiography followed by MRI to Dx Stenerlesion. MSK US can be used if MRI is unavailable.
�Stener lesion on MRI & MSUS: ulnar collateral stump is more superficial to Adductor pollicis aponeurosis and appears like a low signal mass-like stump forming so-called “yo-yo on the string sign” reported both on MRI and MSK US.
Rx: often operative
Boxer Fx: m/c MC Fx. An extra-articular usually non-comminuted or minimal comminuted Fx through m/c the 5th and sometimes the 4th MCneck-head junction (occasionally through the shaft) resulting in volar head angulation. Mechanism: direct impact as in clenched fist punching hard surface (e.g., facial bones/wall punching) hence 95% in young males.
Imaging: x-radiography hand series is sufficient
Rad Dx: Fx line transverse or oblique through MCneck with volar head angulation. Evaluate the degree of displacement, critical to report.
N.B. If the same mechanism fractures the 2ndand 3d MC in the same anatomic area, it may require operative care.
Phalangeal hand Fx: m/c skeleton Fx (10% of all Fx). Sports and industrial injuries dominate
Imaging: x-radiography with hand series or PA/lateral finger views will suffice
Rad Dx: if prox phalanx Fx, distal fragment is angled volarly with prox fragment dorsally. Distal phalanx may be angled dorsally. Key observation: nail bed injury, which considered an open Fx with a�risk of infection.
Rx: if <10-degree angulation-buddy-taping with motion rehab. CRPP vs. ORIF can be considered in complex cases-Orthopedic hand surgeon referral
Complication: loss of motion, necrosis, infection.May result with amputation
For additional common injuries: PIP is m/c dislocated joint. Mullet (Baseball) finger, Jersey finger and other injury refer to:
Felon: septic infection of the fingertip pulp typically with Staph.Aureus. Causes: needle prick(diabetics), paronychia, nail splinters, etc. m/c in index and thumb, presenting with pain, swelling, etc.
D/t specific pulp anatomy theinfection>swelling leads to pulp compartment syndrome-pressure and necrosis.
Rx: operative with incision distal to DIP, irrigation/debridement
Pediatric Wrist Injury
Incomplete Fx: Greenstick Fx, Torus (Buckle)Fx, Bowing (Plastic) deformity/Fx. D/t FOSHe.g. fell off the monkey bar. m/c affects <10-years-old.
Rx: usually non-operative (closed reduction and casting)
Distal Radioulnar Joint (DRUJ) Instability-common injury following trauma as in FOOSHwith wrist hyperextension and rotation and disruption of DRUJ ligaments and TFCcomplex. Avulsion of ulnar styloid with the�dorsal or volar displacement of distal ulnar should be noted.
Imaging steps: x-rays initially, MRI may identify ligaments and TFC damage, MSKUScan help with ligaments tearing.
Wrist DJD-typically is secondary to trauma, scapholunate dissociation, SLAC, SNAC wrist, CPPD, Keinboch or Preiser Disease and others.
May lead to major functional loss
Imaging: typically presents as radiocarpal JSL, subchondral sclerosis,osteophytosis, subcortical cysts, and loose bodies. Typically additional induces intercarpal degeneration and particularly Tri-scaphe joint.
MRI may be helpful with early recognition of scapholunate dissociation, Lunate/Navicular AVN.
If isolated MCP OA noted considerCPPD & Hemochromatosis (Hook-like osteophytes)
Clinically:
Mid-age females
Typically painless except 1st CMC OA
DIPs-Heberden nodes, PIPs-Bouchard nodes
Erosive OA (occasionally called�inflammatory OA�)
A Spectrum of OA but producing central proximal erosions at DIPs and PIPsresulting with very characteristic �gullwing� appearance. No systemic inflammation (no CRP, RF, Anti-CCP Ab)typically in middle-aged/elderly females, like Hand OA, often seen in families
Rheumatoid Arthritis
Rheumatoid Arthritis (RA)-chronic systemic inflammatory disease of unknown etiology, targeting synovial joints, tendons with multiple systemic involvement (lung, CVS, Ocular, Skin, etc.) Pathology: Tcell>Macrophage/APC>mediatedautoimmune process resulting in pannus formation and gradual destruction of ST, cartilage, bone,�and other tissues. 3% FemalesVS.1% Males. Environmental triggers: infection, trauma, smoking,�and others in a genetically susceptible individual. 20-30%may be disabled after 10-years.
In adults: Radial head Fx is the m/c (33%) and accounts for 1.5-4% of all fractures. Etiology: FOOSH with forearm pronated. Associated injuries: elbow collateral ligaments tears. EssexLoprestiFx with interosseous membrane tearing and dislocation of the Distal Radio-Ulnar Joint(DRUJ)
Terrible triad: of the Radial head Fx, elbow dislocation and Coronoid process Fx (typically avulsed by the Brachialis M)
Imaging: 1st step is x-radiography with elbow series, CT scanning may help in complex cases, MRIif ligamentous injury.
In children: Supracondylar Fx of the distal humerus accounts for 90% of acute trauma. It is always d/t accidental trauma with FOOSH and elbow extended, rarely <5% with flexed elbow. MostSupracondylar Fx occur in children <10 y.o. Males>Females. Complications: malunion in cubitus varus aka Gunstock deformity, vascular injury and acute ischemic compartment syndrome with Volkmann contracture
Imaging: 1st step x-radiography can be sufficient. CT occasionally used in complex cases.
Radial head (RH) Fx: Mason classification helps to determine the degree of complexity and mode of treatment
Type 1- undisplaced is the m/c and stable contained by ligaments. On radiographs can be very subtle and evaluation of abnormal elbow fat pads is critical and often the only diagnostic clue
Type 2- displaced by 2-mm or > with rotational block
Type 3- comminuted >2-3 fragments and
Type4 is presented with RH fx, posterior elbow dislocation and sometimes Coronoid process fracture often d/t Brachialis M avulsion
Rx: Type 1 managed non-operatively by immobilization and movement rehab. Type 2- ORIF if rotational block. Type 3 and 4, ORIF and RH resection or RH arthroplasty
Note abnormally displaced anterior fat pad (orange arrow) and the emergence of the posterior fat pad (green arrow) that is usually deep in the olecranon fossa and not seen unless acute hemarthrosis or other effusiondevelopsFat pad signs are most reliable indicators of intra-articular elbow Fx
Mason type 1 RH Fx can be v. subtle and missed. Radiographic search should involve a�close evaluation of positive fat pad signs. Note anterior fat pad displacement aka Sail sign and the presence of the post fat pad d/t acute bleed
Monteggia fracture-dislocations: prox 1/3ulnar shaft Fx. with concomitant dislocation of PRUJ (radial head). FOOSH injury. Children4-12 y.o. Infrequent in adults.
X-rays readily reveal ulnar Fx, but radial head dislocation may be subtle and occasionally missed. This is a serious injury leading to elbow disability if Dx delayed 2-3 weeks or left untreated. X-rays are typically sufficient:Rx: casting vs. operative.
Supracondylar Fx: this is the M/C elbow Fx in children.
Especially, the un-displaced types 1(top right) is difficult to Dx. Abnormality of “fat pads” and anterior humeral line and radiocapitella line disturbance are often most reliable
Type 3 carries a particularly high risk for Volkmann contracture (vascular ischemic-necrosis of the anterior forearm muscle compartment
Elbow complaints in a young athlete
Epicondyle Fx: common pediatric injury, about 10%.Essentially an avulsion Fx and a MUCL tear. Medial epicondyle is m/c Fx. FOOSH is the m/c mechanism.M>F. If minimally displaced or undisplaced can be treated with casting esp. in non-dominant arm. If displaced as in this case, require ORIF.
Medial epicondyle avulsive Fx in a young baseball pitcher was coined a �little league elbow� in the 60sand now should be avoided to avoid confusion
OCD of the Capitellum is a common athletic injury induced by repeated compression/flexion. OCD must be DDx from Panner�s disease or osteochondritis typically presented in younger patients
Difficulty in diagnosis may stem�from multipleapophysis about the elbow (see CRITOE)
Imaging: 1st step: x-rays followed by MRI and MRarthrogramme if indicated.
CT may help with complex injury evaluation. MRI and MSKUS may help with a�ligament injury.
Elbow Arthritis
DJD of the elbow is uncommon and typically 2nd to trauma, occupation, CPPD, OCD of theCapitellum or other pathology. Clinically: pain, reduced ROM esp. in dominant arm, deterioration of ADL. Loss of terminal flexion and extension. 50% develop Ulnarcompressive neuropathy. Rx: conservative,arthroscopic debridement/osteophytes removal, capsular release. In older patients and not active patients Total Elbow Arthroplasty (TEA) can be used
Imaging: x-radiography is sufficient, CT helps with pre-operative planning
Inflammatory Arthritis: RA of the elbow is frequent (20-50%) and destructive d/t synovitis, pannus, bone/cartilage,�and ligamentous destruction/laxity. Clinically: begins after the onset of hands symptoms with, symmetrical swelling, pain, reduced ROM, flexion contracture. Presence of rheumatoid nodules can be noted along the olecranon and posterior forearm. Rx: DMARD, operative tendons repair.
Imaging: x-radiography with early non-specific effusion (fat pads),later: erosions, symmetric JSL, osteopenia. MSK US helps early Dx. MRI reveals synovitis; bone edema correlates with pre-erosive x-ray findings, synovial enhancement on FS T1+C.
Gouty Arthritis: may affect the elbow but less than in the lower extremity. Olecranon bursitis causing a �rising sun sign� on x-rays with or w/o bone erosions. Aspiration and polarised microscopy revealing needle-shaped negatively birefringent monosodium urate crystals. Rx: colchicine, other meds.
Septic Arthritis: consider in people with diabetes, IV drug users, concurrent RA, patients with active TB, gonococcal in young adults. Clinically presents as monoarthritis with or w/o constitutional signs. X-ray: poor detection in early stages. US may show effusion and high Doppler.MRI: effusion, osseous edema. Bone scintigraphy can help as well. Labs: CBC, ESR, CRP. Diagnostic arthrocentesis with gram staining and culture are crucial. Rx: Prompt IV antibiotics
Juvenile Idiopathic Arthritis (JIA) considered M/C chronic disease of childhood and preceded IBD infrequency. Dx is clinical and imaging: Criteria: Joint pain and swelling in a child 0-16-years for 6-weeks or longer. Many forms exist�M/C pauciarticular(oligoarticular) 40%, F>M, associated with ocular involvement (iridocyclitis) and potential blindness. Polyarticular and Systemic forms.
Elbow is frequently affected along with the knee, wrists,�and hands,�especially in polyarticular dz.
Labs: ESR/CRP RF-VE in most cases
Imaging: early x-ray features are non-specific. Later: osseous erosion, destruction of joint cartilage, overgrowth of articular epiphyses, early closure of physis. Delayed features: 2nd DJD, joint ankyloses.DDx: hemophilic arthropathy. Cervical radiographs are crucial.
Rx: DMARD, conservative care
Miscellaneous pathologies
Supracondylar process: 2% of the population. Described by Sir JohnStruthers in 1854. Fibrous band(Ligament of Struthers) may lead to compression of the Median N. DDx fromOsteochondroma that typically points away from the joint
Primary synovial chondrometaplasia�(Reichel Syndrome): abnormalmetaplasia of synovial cells shedding cartilage into joint potentially causing DJD, extrinsic bone erosion, synovitis, nerve compressions etc. Removedoperatively. Imaging: multiple osseocartilaginous loose bodies of relatively equal sizes in the joint cavityDDx with DJD and 2ndosteochondromatosis. MRI-low signal onT1 and T2 with potential joint effusion. Ina tight joint like the elbow may present with large joint distention.�
Panner�s Disease: osteochondrosis of theCapitellum typically in 5-10 y.o. young athlete DDX from OCD of Capitellum(discussed) that occurs in teenagers.Clinically: pain on activity. Recovery occurs in most cases by spontaneous healing. Imaging: x-rays reveal sclerosis and slight fragmentation of theCapitellum w/o loose body. MRI: low T1and high T2 signal in the entireCapitellum.
Myositis Ossificance:
Soft Tissue & Bone Neoplasms about the Elbow
Lipoma: intramuscular, subcutaneous. Most common soft tissue neoplasms. Composed of fat but a substantial number may undergo fat necrosis-calcification-fibrosis. Typically remains benign. Occasionally difficult to DDx from a well-differentiated liposarcoma. Imaging: x radiography: radiolucent lesion well-circumscribed with or w/o calcification. US and MRI are important. On MRIT1high, T2 low SI.
Hemangioma: benign vascular lesion, often composed of multiple vascular channels. Capillary vs. cavernous. More common in children, but found in any age. May often form phleboliths (calcification). Imaging: x-rays reveal soft tissue mass containing phleboliths. MRI: T1-high or variable signal. T2-high signal in areas of slow flow. �bag of worms� sign. Biopsy best avoided. Rx: difficult: local excision vs. embolization vs. observation. High recurrence.
Peripheral Nerve sheath tumor (PNST): benign vs.malignant. Greater incidence in NF1 with a higher risk of malignant PNST. Benign PNST: Schwannoma vs.Neurofibroma. Spinal vs. peripheral nerves. Histology: Schwann cells interspersed with fibroblast and vessels.Clinically: pts in 20s and 30s, palpable mass with or w/o local pressure. Imaging: MRI: T1: split-fat sign, T2: target sign. T1+C enhancement
Soft Tissue Sarcomas: MFH, Synovial sarcoma,(discussed), Liposarcoma (more frequent in the retroperitoneum) Dx: MRI. Clinically: Dx is delayed d/t painless enlarging mass often ignored. Clinically palpable mass deserves MRI examination, US may be helpful. Biopsy confirms Dx.
Malignant bone Neoplasms: Children: OSA, Ewing�s sarcoma (discussed) Adults: Mets, Myeloma (discussed)
Proximal humeral Fx account for 4-6% of all Fxs. Osteoporotic (OSP) Fx in >60 y.o associated with minimal trauma with F: M 2:1 ratio. In young patients, acute high energy trauma predominates.
Complications: AVN humeral head, Axillary N paralysis.
Neer Classification: considers fractures along 4-anatomical lines with or w/o displacement >1-cm & 45-degree angulation
One part Neer Fx- no displacement or very minimal <1-cm/45-degree. Can affect 1-4 lines and M/C at greater tuberosity. 80% of proximal humeral Fx are one-part Neer.
Two-part Fx: 1-part is displaced >1-cm/45-degrees. m/c involves the surgical neck
Three-part Fx: 2-parts are displaced >1-cm/45-degrees.
Four-part Fx: all 4-parts can be displaced. Uncommon <1%
Imaging: 1st step-radiography, CT may be used in more complex cases. Orthopedic referral
Management: Neer one-part Fx is treated with Sling Immobilisation and progressive rehab
The vast majority of Fx in the elderly are treated non-operatively
Younger patients (40-65) may occasionally require hemiarthroplasty if 3 or 4-part Neer Fx present. Greater risk of AVN
Proximal Humerus Fractures
Note: Left image: Fx involving the anatomical neck and the greater tuberosity with minimal displacement <1-cm/45-degree thus Dx as one-part Fx. Right image: Small avulsion Fx of the greater tuberosity with significant displacement (>45-degrees & 1-cm) thus Dx as two-part Fx
Note: three-part Neer Fx (left) and four-part Neer Fx (right)> Management: operative in most cases in younger (40-65) patients
Refers to complete separation of the humerus from scapula glenoid. In 20-40s M: F 9:1 ratio, in60-80S M: F 3:1
Anatomy: Shoulder stability is sacrificed for mobility, and overall GHJD is the m/c among large joints in the body
Protective falls (e.g., FOOSH) and MVA are m/c causes. GHJ is most vulnerable in abduction, extension and external rotation. Anatomical factors: shallow glenoid, laxed ant-inferior capsule and GH ligaments. GHJD will induce severe tearing of major GHJ restraints. Associated osseous and labral injuries are common and may lead to chronic instability, DJD,�and functional changes
3-types: Anterior GHJD (95%)
Posterior GHJD (4%) especially associated with epileptic seizures, electrocution and can occur b/l
Inferior GHJD aka Laxatio Erecta (<1%) associated with severe trauma
Clinically: AGHJD presents with severe pain, the arm is externally rotated and adducted, severe limitation of movement. GHJD may persist as chronic dislocation.
Management: prompt reduction in ED under anesthesia or heavy sedation with Kocher technique top image (not used), External rotation method (middle) or Milch technique (can be used w/o anesthesia) and a few other methods. Delay in reduction correlates with greater risk of immediate and long-term�complications
Diagnostic Imaging Approach
Shoulder series x-radiography is sufficient. Additional Imaging with CT scanning and MRI may be helpful to Dx osseous, cartilage, labral/ligaments pathology
Anterior GHJD (95%). Subcoracoid position(top right) of the humerus is the m/c
Anterior GHJD may also occur as subglenoid(bottom left)and infrequently as subclavicular
Key to radiographic search is to evaluate associated Bankart and Hill-Sachs injuries
Bankart Lesion
Occurs during anterior GHJD d/t impaction of the head into anterior-inferior glenoid. Variations exist (see next slide). BonyBankart can be seen on x-rays. So-called soft tissue Bankart requires MRI. Cartilage (soft)Bankart is the m/c.
Hill-Sachs aka Hatchet deformity (arrow postreduction)occurs during the same mechanism as Bankart, i.e., compression and impaction of posterolateral aspect of the head against the glenoid producing wedge-shape Fx. Hill-Sachs lesion may predispose to recurrent/chronic GHJD.
Bankart lesion may heal, but operative suture anchors are needed sometimes
CT arthrogram and MRI may be helpful
Types of Bankart Lesion
Note different types of Bankart lesion. Onlyosseous Bankart can be seen radiographically. Soft tissue Bankart requires MRI with and without intra-articular gadolinium(arthrogram).
Posterior Dislocation
Note: posterior GHJD with its characteristic signs:
Trough sign aka reverse Hill-Sachs. Occurs d/t anterolateral head impaction Fx
Rim sign: only occurs in the PGHJD d/t posterior position of the head and anterior glenoid-to humeral head distance 6-mm or greater
Light-bulb sign: d/t acute internal rotation of the humerus (head)
Inferior GHJD
Inferior GHJD aka Laxatio Erecta
Severe hyperabduction and inferior displacement of the humerus. Greater chances of severe neurovascular injury and acromial Fx
The dislocated arm is hyperabducted and fixed with the elbow flexed and the arm above the head
ACJ Dislocation (ACJD)
ACJD: common injury, 9% of shoulder girdle injuries esp. in male athletes by a direct blow
Rockwood classification (left) evaluates tearing of AC and CC ligaments and regional muscles
Type1, 2, 3 among the m/c
Type 1: sprain of ACL w/o tearing
Type 2: tear of ACL and sprain of CCL
Type 3: tear of AC & CCL. The clavicle is elevated above the acromion. If <2-cm good results with conservative Rx.
Imaging: x-radiography with b/l ACJ views with and w/o weights to compare both ACJs. In complex cases CT scanning esp. if Fx is considered
Management: Type 3 (>2-cm) & Types 4-6Operative
Type 3 ACJ Separation
Type 3 ACJ separation (top left)
More significant ACJD (bottom images) with clinical sign of acromion under the skin and resultant ORIF
Rotator Cuff Muscles (RCM) Pathology
RCM tendinopathy: collagenous degeneration of RCM particularly Supraspinatus M. tendon(SSMT) d/t overuse/degeneration-micro tearing with collagenous replacement. Impingement syndrome is a 2nd extrinsic cause. Presented clinically as pain and limited ROM
Imaging Dx: MSK US can be as accurate as MRI and better in some cases d/t dynamic evaluation v. cost effective
Key MRI clue is thickened inhomogeneous SSMTwith increased signal on all pulse sequences d/t fatty degeneration and inflammation (left images: T1 & T2 FS)
MSKUS findings: thickening of the SSMTsubstance with a change�in normal echogenicity.MSKUS is good to DDx with SSMT tears. US advantages are that it allows dynamic evaluation of painful structures
Partial tear of SSMT: partial (incomplete) tear ofSSMT may occur at the bursal and articular surface or interstitial, i.e., intra-substance/noncommunicating. Etiology: sub-acromial impingement, acute strain, and chronic microtrauma tendinosis
Clinically: pain on abd and flexion, impingement tests, Hawkins-Kennedy tests, etc. Pearls: partial tears can be more painful than complete tears
Imaging Dx: MSKUS is as good as MRI (N.B.some studies indicated MSKUS is more superior to MRI). Key MRI findings: gap/incomplete tear of SSMT filled with joint fluid +/- granulation tissue
MSKUS: decreased echogenicity of SSMT, thinning and partial tearing filled with fluid(anechoic areas arrows). Lost convexity of tendon bursal or articular interface.
Full Thickness SSMT (rot cuff) tear: degeneration/tearing of rot cuff. 2nd to impingement by Hooked acromion, overhead overuse or acute trauma. 7-25% of shoulder pain in the general population. Clinically: pain on impingement tests.
Imaging Dx: MSKUS is as good as MRI.Limitations: poor Dx of labral pathology. Key USDx: focal tendon interruption, an anechoic gap (fluid filled), hypoechoic tendon, tendon retraction, uncovered cartilage sign (bottom left, A: US B: MRI)
MRI: key Dx: insertional tear extending through entire SSMT crescent, retraction with fatty degeneration of SSMT and the muscle. If retraction is at 12 o�clock or greater (top images), it may not be anchored operatively
Rotator Cuff (RTC) Calcific Tendinitis: usually d/t calcium HADD crystals. Middle-aged women are most affected. Ranges from asymptomatic imaging finding to severe destructive arthropathy or Milwaukee shoulder(infrequent)
HADD has 3-pathological phases: formation resting-resorption.Mild-to-moderate pain esp. in resting phase.
Imaging: x-radiography: homogenous ovoid mineralization within RTCMT, m/c in SSMT. MRI: ovoid/globular decreased signal on all pulse sequences often with surrounding edema (bottom left)
Rx: self-resolution occurs. Advanced cases: operative aspiration etc.
Superior Labrum Anterior to Posterior (SLAP) Lesions/Tears
SLAP tears: FOOSH and throwing sports or chronic shoulder instability aka Multidirectional shoulder instability (in 20%). Type 1-9 exist but the M/C areType 1-4
In all 4-types superior labrum is affected with or w/oLHBMT anchor tear (see pictures). Clinically: pain, limitation of AROM with active compression tests, typically non-specific findings mimicking RTCpathology
Imaging is crucial: best imaging is MRI arthrography. Key signs: hyperintense linear fluid signal within superior labrum +/- extending along the LHBT on fat-suppressed fluid sensitive imaging and FS T1 arthrogram. Best observed on coronal slices.
Rx: small tears may heal, but unstable tears require operative care.
Key DDx: anatomical variants like Buford complex andSub-labral foramen
SLAP tear with a paralabral cyst (bottom right)
Normal variant DDx: sub labral foramen(bottom left) note: MR arthrography with contrast undercutting the labrum but w/o extending posteriorly to the LHBT
Shoulder Arthritis
GHJ DJD: usually associated with a 2nd cause: trauma, instability, AVN, CPPD, etc. Presented with pain, crepitus and decreased ROM/function. Associated RTC disease may be present. Imaging; x-radiography is sufficient and provides grading/care planning.Major findings: joint narrowing, osteophytosis esp. at the inferior-medial head (orange arrow), subchondral sclerosis/cysts. Often noted superior head migration d/t RTC disease.
ACJ OA: common and typically primary with aging. Presents with ACJ loss and osteophytes. Osteophytes along the undersurface of the ACJ �keel osteophytes�(blue arrow) may lead to RTC muscle tear. Regional bursitis is other clinical feature of ACJ arthrosis.
Management: usually conservative depending on clinical signs/symptoms
Rheumatoid Arthritis GHJ: RA is a multisystem inflammatory disease affecting multiple joints lined by the synovium. GHJ RA is common (m/c large joints in RA knees/shoulders). Clinically: pain, limited ROM and instability, muscle weakness/wasting. Hands, feet,�and wrists are m/c affected. Imaging: x-radiography reveals periarticular erosions, uniform joint space loss, juxta-articular osteoporosis, subluxations,�and soft tissue swelling. MRI can help detect�commonly associated RTC tearing and instability. Early changes can be detected by MSKUS esp. with power Doppler use indicating hyperemia/inflammation.
Note: L shoulder x-ray revealing cartilage destruction and symmetrical joint loss, multiple erosions, and likely loss of RTCM support with superior head migration, ST effusion present.
Note: PDFS coronal and axial MRI slices of GHJ RA indicating marked inflammatory joint effusion, bone erosion/edema, synovial pannus formation and likely tear in RTC m. Management: Rheumatological referral and pharmacotherapy with DMARD. Operative care asRTCM repair. 10% of patients are disabled d/t RA
Neuropathic Osteoarthropathy aka Charcot’s shoulder: d/t neurovascular and neural periarticular damage. Multiple causes exist.M/c develops in diabetics in midfoot. Shoulder Charcot is m/c in Syringomyelia (25%), trauma paralysis, MS, etc. Dx: clinical(50% pain/swelling 50% painless destruction). Imaging is crucial. X-radiography is sufficient in well-established cases, but early Dx is challenging. MRI may help with early Dx and delayed complications. Rad Dx: Shoulder Charcot is m/c presented as atrophic type destructive arthropathy with humeral head appearing as if surgically amputated along with intra-articular debris, density, distention, dislocation, and other key features
Septic Shoulder: shoulder is the 3rd m/c followingknee>hips. Patients at risk: diabetics, RA pts, immunocompromised, I.V. drug users, indwelling catheters, etc. Routes: hematogenous (m/c), direct inoculation (iatrogenic, trauma etc.) adjacent spread(e.g. OM). Staph. Aureus (>50%) m/c.
Clinically: joint pain and dec. ROM, fever 60% only, toxemia, inc. ESR/CRP. Dx: imaging and joint aspiration/culture. RadDx: early x-rays often unremarkable except ST effusion/fat planes obscuration, joint widening. Later7-12 days patchy osteopenia, moth-eaten/permeating bone resorption, articular destruction, joint narrowing. May progress to severe joint destruction and ankyloses. Early Dx & I.V. antibiotics are crucial even before culture. Operative irrigation and joint drainage in some cases. Complications are possible esp. if Rx is delayed. MSKUS with needle aspiration may help. Note: (top image) non-traumatic joint widening with inferolateral head displacement d/t septic A dx: by needle aspiration Staph. Aures.
Ischemic Osteonecrosis
Ischemic Osteonecrosis of the humeral head may occur d/t trauma (Neer four-part Fx), Steroids, Lupus, Sickle cell, Alcoholism, Diabetes,�and many other conditions. Imaging is crucial: MRI detects earliest changes as intraosseous edema. X-ray features are late, presented as a collapse of subchondral bone with sclerosis �snow cap� sign, fragmentation, and progressive severe DJD
Management: orthopedic referral, core decompression in early cases, hemiarthroplasty in moderate and total arthroplasty in severe cases.
Shoulder Neoplasms
In adults >40, bone Mets d/t lung, breast, renal cell, thyroid CA & prostate are the m/c causes. Clinically: may mimic pain resemblingRTC/joint changes. Should be evaluated carefully. Key to Dx: Hx, PE and Imaging esp.in pts with known primary
Imaging: 1st step x-rays, MRI can help, Tc99bone scintigraphy helps to detect regional and distant disease. X-ray features: destructive lytic changes typically in prox humerus(red marrow) with or w/o path Fx. DDx: Mets, MM, lymphoma
Clinically: night pain, pain at rest, etc. Lab tests: unrewarding, in severe cases hypercalcemia may be noted.
Primary Malignant bone neoplasms (shoulder) Adults: M. Myeloma or Solitary plasmacytoma, Chondrosarcoma may transform from an enchondroma and some others. In children/teenagers: OSA vs. Ewing�s
Primary benign bone neoplasms (shoulder). Adults: Enchondroma (patients in their 20-30s)GCT. In children: Simple bone cyst (Unicameral Bone cyst), Osteochondroma, Aneurysmal Bone Cyst, Chondroblastoma (rare)
Imaging: 1st step x-radiography
MRI is essential to Dx. Especially in cases of primary malignant neoplasms Evaluate extent, soft tissue invasion, preoperative planning, staging, etc.
About 1.5 million people in the United States have rheumatoid arthritis. Rheumatoid arthritis, or RA, is a chronic, autoimmune disease characterized by pain and inflammation of the joints. With RA, the immune system, which protects our well-being by attacking foreign substances like bacteria and viruses, mistakenly attacks the joints. Rheumatoid arthritis most commonly affects the joints of the hands, feet, wrists, elbows, knees and ankles. Many healthcare professionals recommend early diagnosis and treatment of RA.
Abstract
Rheumatoid arthritis is the most commonly diagnosed systemic inflammatory arthritis. Women, smokers, and those with a family history of the disease are most often affected. Criteria for diagnosis include having at least one joint with definite swelling that is not explained by another disease. The likelihood of a rheumatoid arthritis diagnosis increases with the number of small joints involved. In a patient with inflammatory arthritis, the presence of a rheumatoid factor or anti-citrullinated protein antibody, or elevated C-reactive protein level or erythrocyte sedimentation rate suggests a diagnosis of rheumatoid arthritis. Initial laboratory evaluation should also include complete blood count with dif- ferential and assessment of renal and hepatic function. Patients taking biologic agents should be tested for hepatitis B, hepatitis C, and tuberculosis. Earlier diagnosis of rheumatoid arthritis allows for earlier treatment with disease-modifying antirheumatic agents. Combinations of medications are often used to control the disease. Methotrexate is typically the first-line drug for rheumatoid arthritis. Biologic agents, such as tumor necrosis factor inhibitors, are generally considered second-line agents or can be added for dual therapy. The goals of treatment include minimiza- tion of joint pain and swelling, prevention of radiographic damage and visible deformity, and continuation of work and personal activities. Joint replacement is indicated for patients with severe joint damage whose symptoms are poorly controlled by medical management. (Am Fam Physician. 2011;84(11):1245-1252. Copyright � 2011 American Academy of Family Physicians.)
Rheumatoid arthritis (RA) is the most common inflammatory arthritis, with a lifetime prevalence of up to 1 percent worldwide.1 Onset can occur at any age, but peaks between 30 and 50 years.2 Disability is common and significant. In a large U.S. cohort, 35 percent of patients with RA had work disability after 10 years.3
Etiology and Pathophysiology
Like many autoimmune diseases, the etiology of RA is multifactorial. Genetic susceptibility is evident in familial clustering and monozygotic twin studies, with 50 percent of RA risk attributable to genetic factors.4 Genetic associations for RA include human leukocyte antigen-DR45 and -DRB1, and a variety of alleles called the shared epitope.6,7 Genome-wide association studies have identified additional genetic signatures that increase the risk of RA and other autoimmune diseases, including STAT4 gene and CD40 locus.5 Smoking is the major environmental trigger for RA, especially in those with a genetic predisposition.8 Although infections may unmask an autoimmune response, no particular pathogen has been proven to cause RA.9
RA is characterized by inflammatory pathways that lead to proliferation of synovial cells in joints. Subsequent pannus formation may lead to underlying cartilage destruction and bony erosions. Overproduction of pro-inflammatory cytokines, including tumor necrosis factor (TNF) and interleukin-6, drives the destructive process.10
Risk Factors
Older age, a family history of the disease, and female sex are associated with increased risk of RA, although the sex differential is less prominent in older patients.1 Both current and prior cigarette smoking increases the risk of RA (relative risk [RR] = 1.4, up to 2.2 for more than 40-pack-year smokers).11
Pregnancy often causes RA remission, likely because of immunologic tolerance.12 Parity may have long-lasting impact; RA is less likely to be diagnosed in parous women than in nulliparous women (RR = 0.61).13,14 Breastfeeding decreases the risk of RA (RR = 0.5 in women who breastfeed for at least 24 months), whereas early menarche�(RR = 1.3 for those with menarche at 10 years of age or younger) and very irregular menstrual periods (RR = 1.5) increase risk.14 Use of oral contraceptive pills or vitamin E does not affect RA risk.15
Diagnosis
Typical Presentation
Patients with RA typically present with pain and stiffness in multiple joints. The wrists, proximal interphalangeal joints, and metacarpophalangeal joints are most commonly involved. Morning stiffness lasting more than one hour suggests an inflammatory etiology. Boggy swelling due to synovitis may be visible (Figure 1), or subtle synovial thickening may be palpable on joint examination. Patients may also present with more indolent arthralgias before the onset of clinically apparent joint swelling. Systemic symptoms of fatigue, weight loss, and low-grade fever may occur with active disease.
Diagnostic Criteria
In 2010, the American College of Rheumatology and European League Against Rheumatism collaborated to create new classification criteria for RA (Table 1).16 The new criteria are an effort to diagnose RA earlier in patients who may not meet the 1987 American College of Rheumatology classification criteria. The 2010 criteria do not include presence of rheumatoid nodules or radiographic erosive changes, both of which are less likely in early RA. Symmetric arthri- tis is also not required in the 2010 criteria, allowing for early asymmetric presentation.
In addition, Dutch researchers have developed and validated a clinical prediction rule for RA (Table 2).17,18 The purpose of this rule is to help identify patients with undifferentiated arthritis that is most likely to progress to RA, and to guide follow-up and referral.
Diagnostic Tests
Autoimmune diseases such as RA are often characterized by the presence of autoanti- bodies. Rheumatoid factor is not specific for RA and may be present in patients with other diseases, such as hepatitis C, and in healthy older persons. Anti-citrullinated protein antibody is more specific for RA and may play a role in disease pathogenesis.6 Approxi- mately 50 to 80 percent of persons with RA have rheumatoid factor, anti-citrullinated protein antibody, or both.10 Patients with RA may have a positive antinuclear antibody test result, and the test is of prognostic impor- tance in juvenile forms of this disease.19 C-reactive protein levels and erythrocyte sedimentation rate are often increased with active RA, and these acute phase reactants are part of the new RA classification criteria.16 C-reactive protein levels and erythrocyte sedimentation rate may also be used to follow disease activity and response to medication.
Baseline complete blood count with differential and assessment of renal and hepatic function are helpful because the results may influence treatment options (e.g., a patient with renal insufficiency or significant thrombocytopenia likely would not be prescribed a nonsteroidal anti-inflammatory drug [NSAID]). Mild anemia of chronic disease occurs in 33 to 60 percent of all patients with RA,20 although gastrointestinal blood loss should also be considered in patients taking corticosteroids or NSAIDs. Methotrexate is contraindicated in patients with hepatic disease, such as hepatitis C, and in patients with significant renal impairment.21 Biologic therapy, such as a TNF inhibitor, requires a negative tuberculin test or treatment for latent tuberculosis. Hepatitis B reactivation can also occur with TNF inhibitor use.22 Radiography of hands and feet should be performed to evaluate for characteristic periarticular erosive changes,�which may be indicative of a more aggressive RA subtype.10
Differential Diagnosis
Skin findings suggest systemic lupus erythematosus, systemic sclerosis, or psoriatic arthritis. Polymyalgia rheumatica should be considered in an older patient with symptoms primarily in the shoulder and hip, and the patient should be asked questions related to associated temporal arteritis.
Chest radiography is helpful to evaluate for sarcoidosis as an etiology of arthritis.�Patients with inflammatory back symptoms, a history of inflammatory bowel disease, or inflammatory eye disease may have spondyloarthropathy. Persons with less than six weeks of symptoms may have a viral process, such as parvovirus. Recurrent self-limited episodes of acute joint swelling suggest crystal arthropathy, and arthrocentesis should be performed to evaluate for monosodium urate monohydrate or calcium pyrophosphate dihydrate crystals. The presence of numerous myofascial trigger points and somatic symptoms may suggest fibromyalgia, which can coexist with RA. To help guide diagnosis and determine treatment strategy, patients with inflammatory arthritis should be promptly referred to a rheumatology subspecialist.16,17
Rheumatoid arthritis, or RA, is the most common type of arthritis. RA is an autoimmune disease, caused when the immune system, the human body’s defense system, attacks its own cells and tissues, particularly the joints. Rheumatoid arthritis is frequently identified by symptoms of pain and inflammation, often affecting the small joints of the hands, wrists and feet. According to many healthcare professionals, early diagnosis and treatment of RA is essential to prevent further joint damage and decrease painful symptoms. Dr. Alex Jimenez D.C., C.C.S.T. Insight
Treatment
After RA has been diagnosed and an initial evaluation performed, treatment should begin. Recent guidelines have addressed the management of RA,21,22 but patient preference also plays an important role. There are special considerations for women of childbearing age because many medications have deleterious effects on pregnancy. Goals of therapy include minimizing joint pain and swelling, preventing deformity (such as ulnar deviation) and radiographic damage (such as erosions), maintaining quality of life (personal and work), and controlling extra-articular manifestations. Disease-modifying antirheumatic drugs (DMARDs) are the mainstay of RA therapy.
DMARDs
DMARDs can be biologic or nonbiologic (Table 3).23 Biologic agents include monoclonal antibodies and recombinant receptors to block cytokines that promote the inflammatory cascade responsible for RA symptoms. Methotrexate is recommended as the first- line treatment in patients with active RA, unless contraindicated or not tolerated.21 Leflunomide (Arava) may be used as an alternative to methotrexate, although gastrointestinal adverse effects are more common. Sulfasalazine (Azulfidine) or hydroxychloroquine (Plaquenil) pro-inflammatory as monotherapy in patients with low disease�activity or without poor prognostic features (e.g., seronegative, non-erosive RA).21,22
Combination therapy with two or more DMARDs is more effective than monotherapy; however, adverse effects may also be greater.24 If RA is not well controlled with a nonbiologic DMARD, a biologic DMARD should be initiated.21,22 TNF inhibitors are the first-line biologic therapy and are the most studied of these agents. If TNF inhibitors are ineffective, additional biologic therapies can be considered. Simultaneous use of more than one biologic therapy (e.g., adalimumab [Humira] with abatacept [Orencia]) is not�recommended because of an unacceptable rate of adverse effects.21
NSAIDs and Corticosteroids
Drug therapy for RA may involve NSAIDs and oral, intramuscular, or intra-articular corticosteroids for controlling pain and inflammation. Ideally, NSAIDs and corticosteroids are used only for short-term management. DMARDs are the preferred therapy.21,22
Complementary Therapies
Dietary interventions, including vegetarian and Mediterranean diets, have been�studied in the treatment of RA without convincing evidence of benefit.25,26 Despite some favorable outcomes, there is a lack of evidence for the effectiveness of acupuncture in placebo-controlled trials of patients with RA.27,28 In addition, thermotherapy and therapeutic ultrasound for RA have not been studied adequately.29,30 A Cochrane review of herbal treatments for RA concluded that gamma-linolenic acid (from evening primrose or black currant seed oil) and Tripterygium wilfordii (thunder god vine) have potential benefits.31 It is important to inform patients that serious adverse effects have been reported with use of herbal therapy.31
Exercise and Physical Therapy
Results of randomized controlled trials sup- port physical exercise to improve quality of life and muscle strength in patients with RA.32,33 Exercise training programs have not been shown to have deleterious effects on RA disease activity, pain scores, or radiographic joint damage.34 Tai chi has been shown to improve ankle range of motion in persons with RA, although randomized trials are limited.35 Randomized controlled trials of Iyengar yoga in young adults with RA are underway.36
Duration of Treatment
Remission is obtainable in 10 to 50 percent of patients with RA, depending on how remission is defined and the intensity of therapy.10 Remission is more likely in males, nonsmokers, persons younger than 40 years, and in those with late-onset disease (patients older than 65 years), with shorter duration of disease, with milder disease activity, without elevated acute phase reactants, and without positive rheumatoid factor or anti-citrullinated protein antibody findings.37
After the disease is controlled, medication dosages may be cautiously decreased to the minimum amount necessary. Patients will require frequent monitoring to ensure stable symptoms, and prompt increase in medication is recommended with disease flare-ups.22
Joint Replacement
Joint replacement is indicated when there is severe joint damage and unsatisfactory control of symptoms with medical management. Long-term outcomes are support, with only 4 to 13 percent of large joint replacements requiring revision within 10 years.38 The hip and knee are the most commonly replaced joints.
Long-Term Monitoring
Although RA is considered a disease of the joints, it is also a systemic disease capable of involving multiple organ systems. Extra-articular manifestations of RA are included in Table 4.1,2,10
Patients with RA have a twofold increased risk of lymphoma, which is thought to be caused by the underlying inflammatory�process, and not a consequence of medical treatment.39 Patients with RA are also at an increased risk of coronary artery disease, and physicians should work with patients to modify risk factors, such as smoking, high blood pressure, and high cholesterol.40,41 Class III or IV congestive heart failure (CHF) is a contraindication for using TNF inhibitors, which can worsen CHF outcomes.21 In patients with RA and malignancy, caution is needed with continued use of DMARDs, especially TNF inhibitors. Biologic DMARDs, methotrexate, and leflunomide should not be initiated in patients with active herpes zoster, significant fungal infection, or bacterial infection requiring antibiotics.21 Complications of RA and its treatments are listed in Table 5.1,2,10
Prognosis
Patients with RA live three to 12 years less than the general population.40 Increased mortality in these patients is mainly due to accelerated cardiovascular disease, especially in those with high disease activity and chronic inflammation. The relatively new biologic therapies may reverse progression of atherosclerosis and extend life in those with RA.41
Data Sources: A PubMed search was completed in Clinical Queries using the key terms rheumatoid arthritis, extra-articular manifestations, and disease-modifying antirheumatic agents. The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Also searched were the Agency for Healthcare Research and Quality evidence reports, Clinical Evidence, the Cochrane database, Essential Evidence, and UpToDate. Search date: September 20, 2010.
Author disclosure: No relevant financial affiliations to disclose.
In conclusion, rheumatoid arthritis is a chronic, autoimmune disease which causes painful symptoms, such as pain and discomfort, inflammation and swelling of the joints, among others. The joint damage characterized as RA is symmetrical, meaning it generally affects both sides of the body. Early�diagnosis is essential for treatment of RA. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Relieving Knee Pain without Surgery
Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
1. Etiology and pathogenesis of rheumatoid arthritis. In: Firestein GS, Kelley WN, eds. Kelley�s Textbook of Rheu- matology. 8th ed. Philadelphia, Pa.: Saunders/Elsevier; 2009:1035-1086. 2. Bathon J, Tehlirian C. Rheumatoid arthritis clinical and laboratory manifestations. In: Klippel JH, Stone JH, Crofford LJ, et al., eds. Primer on the Rheumatic Dis- eases. 13th ed. New York, NY: Springer; 2008:114-121. 3. Allaire S, Wolfe F, Niu J, et al. Current risk factors for work disability associated with rheumatoid arthritis. Arthritis Rheum. 2009;61(3):321-328. 4. MacGregor AJ, Snieder H, Rigby AS, et al. Characteriz- ing the quantitative genetic contribution to rheumatoid arthritis using data from twins. Arthritis Rheum. 2000; 43(1):30-37. 5. Orozco G, Barton A. Update on the genetic risk fac- tors for rheumatoid arthritis. Expert Rev Clin Immunol. 2010;6(1):61-75. 6. Balsa A, Cabezo?n A, Orozco G, et al. Influence of HLA DRB1 alleles in the susceptibility of rheumatoid arthritis and the regulation of antibodies against citrullinated proteins and rheumatoid factor. Arthritis Res Ther. 2010;12(2):R62. 7. McClure A, Lunt M, Eyre S, et al. Investigating the via- bility of genetic screening/testing for RA susceptibility using combinations of five confirmed risk loci. Rheuma- tology (Oxford). 2009;48(11):1369-1374. 8. Bang SY, Lee KH, Cho SK, et al. Smoking increases rheu- matoid arthritis susceptibility in individuals carrying the HLA-DRB1 shared epitope, regardless of rheumatoid factor or anti-cyclic citrullinated peptide antibody sta- tus. Arthritis Rheum. 2010;62(2):369-377. 9. Wilder RL, Crofford LJ. Do infectious agents cause rheu- matoid arthritis? Clin Orthop Relat Res. 1991;(265): 36-41. 10. Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet. 2010;376(9746):1094-1108. 11. Costenbader KH, Feskanich D, Mandl LA, et al. Smoking intensity, duration, and cessation, and the risk of rheu- matoid arthritis in women. Am J Med. 2006;119(6): 503.e1-e9. 12. Kaaja RJ, Greer IA. Manifestations of chronic disease during pregnancy. JAMA. 2005;294(21):2751-2757. 13. Guthrie KA, Dugowson CE, Voigt LF, et al. Does preg- nancy provide vaccine-like protection against rheuma- toid arthritis? Arthritis Rheum. 2010;62(7):1842-1848. 14. Karlson EW, Mandl LA, Hankinson SE, et al. Do breast- feeding and other reproductive factors influence future risk of rheumatoid arthritis? Results from the Nurses� Health Study. Arthritis Rheum. 2004;50(11):3458-3467. 15. Karlson EW, Shadick NA, Cook NR, et al. Vitamin E in the primary prevention of rheumatoid arthritis: the Women�s Health Study. Arthritis Rheum. 2008;59(11): 1589-1595. 16. Aletaha D, Neogi T, Silman AJ, et al. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative [published correction appears in Ann Rheum Dis. 2010;69(10):1892]. Ann Rheum Dis. 2010;69(9):1580-1588. 17. van der Helm-van Mil AH, le Cessie S, van Dongen H, et al. A prediction rule for disease outcome in patients with recent-onset undifferentiated arthritis. Arthritis Rheum. 2007;56(2):433-440. 18. Mochan E, Ebell MH. Predicting rheumatoid arthritis risk in adults with undifferentiated arthritis. Am Fam Physi- cian. 2008;77(10):1451-1453. 19. Ravelli A, Felici E, Magni-Manzoni S, et al. Patients with antinuclear antibody-positive juvenile idiopathic arthri- tis constitute a homogeneous subgroup irrespective of the course of joint disease. Arthritis Rheum. 2005; 52(3):826-832. 20. Wilson A, Yu HT, Goodnough LT, et al. Prevalence and outcomes of anemia in rheumatoid arthritis. Am J Med. 2004;116(suppl 7A):50S-57S. 21. Saag KG, Teng GG, Patkar NM, et al. American College of Rheumatology 2008 recommendations for the use of nonbiologic and biologic disease-modifying antirheu- matic drugs in rheumatoid arthritis. Arthritis Rheum. 2008;59(6):762-784. 22. Deighton C, O�Mahony R, Tosh J, et al.; Guideline Devel- opment Group. Management of rheumatoid arthritis: summary of NICE guidance. BMJ. 2009;338:b702. 23. AHRQ. Choosing medications for rheumatoid arthritis. April 9, 2008. www.effectivehealthcare.ahrq.gov/ ehc/products/14/85/RheumArthritisClinicianGuide.pdf. Accessed June 23, 2011. 24. Choy EH, Smith C, Dore? CJ, et al. A meta-analysis of the efficacy and toxicity of combining disease-modify- ing anti-rheumatic drugs in rheumatoid arthritis based on patient withdrawal. Rheumatology (Oxford). 2005; 4 4 (11) :1414 -1421. 25. Smedslund G, Byfuglien MG, Olsen SU, et al. Effective- ness and safety of dietary interventions for rheumatoid arthritis. J Am Diet Assoc. 2010;110(5):727-735. 26. Hagen KB, Byfuglien MG, Falzon L, et al. Dietary inter- ventions for rheumatoid arthritis. Cochrane Database Syst Rev. 2009;21(1):CD006400. 27. Wang C, de Pablo P, Chen X, et al. Acupuncture for pain relief in patients with rheumatoid arthritis: a systematic review. Arthritis Rheum. 2008;59(9):1249-1256. 28. Kelly RB. Acupuncture for pain. Am Fam Physician. 2009;80(5):481-484. 29. Robinson V, Brosseau L, Casimiro L, et al. Thermother- apy for treating rheumatoid arthritis. Cochrane Data- base Syst Rev. 2002;2(2):CD002826. 30. Casimiro L, Brosseau L, Robinson V, et al. Therapeutic ultrasound for the treatment of rheumatoid arthritis. Cochrane Database Syst Rev. 2002;3(3):CD003787. 31. Cameron M, Gagnier JJ, Chrubasik S. Herbal therapy for treating rheumatoid arthritis. Cochrane Database Syst Rev. 2011;(2):CD002948. 32. Brodin N, Eurenius E, Jensen I, et al. Coaching patients with early rheumatoid arthritis to healthy physical activ- ity. Arthritis Rheum. 2008;59(3):325-331. 33. Baillet A, Payraud E, Niderprim VA, et al. A dynamic exercise programme to improve patients� disability in rheumatoid arthritis: a prospective randomized con- trolled trial. Rheumatology (Oxford). 2009;48(4): 410-415. 34. Hurkmans E, van der Giesen FJ, Vliet Vlieland TP, et al. Dynamic Exercise programs (aerobic capacity and/or mus- cle strength training) in patients with rheumatoid arthri- tis. Cochrane Database Syst Rev. 2009;(4):CD006853. 35. Han A, Robinson V, Judd M, et al. Tai chi for treat- ing rheumatoid arthritis. Cochrane Database Syst Rev. 2004;(3):CD004849. 36. Evans S, Cousins L, Tsao JC, et al. A randomized con- trolled trial examining Iyengar yoga for young adults with rheumatoid arthritis. Trials. 2011;12:19. 37. Katchamart W, Johnson S, Lin HJ, et al. Predictors for remis- sion in rheumatoid arthritis patients: a systematic review. Arthritis Care Res (Hoboken). 2010;62(8):1128-1143. 38. Wolfe F, Zwillich SH. The long-term outcomes of rheu- matoid arthritis: a 23-year prospective, longitudinal study of total joint replacement and its predictors in 1,600 patients with rheumatoid arthritis. Arthritis Rheum. 1998;41(6):1072-1082. 39. Baecklund E, Iliadou A, Askling J, et al. Association of chronic inflammation, not its treatment, with increased lymphoma risk in rheumatoid arthritis. Arthritis Rheum. 2006;54(3):692-701. 40. Friedewald VE, Ganz P, Kremer JM, et al. AJC editor�s consensus: rheumatoid arthritis and atherosclerotic cardiovascular disease. Am J Cardiol. 2010;106(3): 442-447. 41. Atzeni F, Turiel M, Caporali R, et al. The effect of phar- macological therapy on the cardiovascular system of patients with systemic rheumatic diseases. Autoimmun Rev. 2010;9(12):835-839.
M/C dislocation of the foot at tarsal-metatarsal articulation (Lisfranc joint). Direct impact or landing and plantar or dorsal flexing the foot. Lisfranc ligament holding 2nd MT base and 1st Cu is torn. Manifests with or w/o fracture-avulsion.
Imaging: 1st step: foot radiography in most cases sufficient to Dx. MSK US may help: show disrupted Cu1-Cu2. Ligament and widened space > 2.5mm. MRI may help but not essential. Weight-bearing view aids Dx.
2-types: homolateral (1st MTP joint in contact) and divergent (2-5 MT displaced laterally and 1st MT medially)
Management: operative fixation is crucial
N.B. Atraumatic Lisfranc dislocation is a frequent complication of a diabetic Charcot foot
Osteochondral Injury of the Talus (OCD)
Common. Non-traumatic found in superior-medial talar dome. Traumatic may affect supero-lateral dome.
Clinically: pain/effusion/locking. Imaging is crucial.
1st step: radiography may reveal focal radiolucent concavity/halo, fragment.
MRI helpful esp. if OCD is cartilaginous and to demonstrate bone edema.
Jones Fx: extra-articular Fx of proximal metaphysis of the 5th MT. Prone to non-union. Often fixed operatively.
Pseudo-Jones: intra-articular avulsion of 5th MT styloid/base by eccentric contraction of Peroneus Brevis M. Managed conservatively: boot-cast immobilization. Both Jones & Pseudo-Jones Dx by foot series radiography.
Stress Fx. Calcaneus, 2nd, 3rd, 5th MTs. Repeated loading (running) or “March foot” 2nd/3rd MT. Clinically: pain on activity, reduced by rest. Dx: x-rays often unrewarding earlier. MRI or MSK US may help. Managed: Conservatively. Complications; progress into complete Fx
Turf toe: common athletic hyperextension of 1st MTP-sesamoid/plantar plate complex is tearing. 1st MTP unstable/loose. Managed operatively.
Arthritis of the Foot & Ankle
DJD of the ankle: uncommon a primary OA. Typically develops as 2nd to trauma/AVN, RA, CPPD, Hemophilic arthropathy, Juvenile Idiopathic Arthritis, etc. manifests as DJD: osteophytes, JSL, subchondral cysts all seen on x-rays
Inflammatory Arthritis: RA may develop in the ankle or any synovial joint. Will typically presents with symmetrical Hands/feet RA initially (2nd, 3rd MCP, wrists, MTPs in feet) usually with erosion, uniform JSL, juxta-articular osteopenia, and delayed subluxations.
HLA-B27 spondyloarthropathies: commonly affect lower extremity: heel, ankle esp in Reactive (Reiter). Erosive-productive bone proliferation is a crucial Dx.
Gouty Arthritis: common in the lower extremity. Ankle, mid-foot foot esp 1st MTPs. Initial onset: acute gouty arthritis with ST effusion and no erosions/tophi. Chronic tophaceous gout: peri-articular, intra-osseous punched-out erosions with over-hanging edges, no initial JSL/osteopenia, ST. Tophi may be seen.
Miscellaneous arthropathy: PVNS. Not common. Affects 3-4th decades of life. The result of synovial proliferation with Macrophages and multi-nucleated Giant Cells filled with hemosiderin and fatty accumulation may lead to inflammation, cartilage damage, extrinsic bone erosions. Dx: x-rays are insensity, MRI modality of choice. Synovial biopsy. Management: operative, can be difficult.
Neuropathic Osteoarthropathy
(Charcot’s joint) Common and on the rise d/t epidemic in type 2 DM. May present with pain initially (50% of cases) and painless destructive arthropathy as a late manifestation. Early Dx: delayed. Imaging is crucial: x-rays: initially unrewarding, some SF effusion is seen. MRI helps with early Dx and extremity off-loading. Late Dx: irreversible dislocations, collapse, disability. Note: Lisfrance dislocation in Charcot joint
M/C mid-foot (TM joint) in 40% of cases, ankle 15%. Progression: Rocker-bottom foot, ulcerations, infections, increased morbidity, and mortality.
Early Dx: by MRI is crucial. Suspect it in patients with type 2 DM especially if early non-traumatic foot/ankle pain reported.
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