2016-2.docx

\ Type 1 endoleak Inadequate seal between the device and the aortic wall, either at the proximal end (type 1A) or the distal end (type 1B) Treatment always indicated: \ Endograft extension \ Cuffs \ Balloon moulding \ Endoanchors \ Surgical explantation \ Type 2 endoleak Retrograde flow from side br...

\ Type 1 endoleak Inadequate seal between the device and the aortic wall, either at the proximal end (type 1A) or the distal end (type 1B) Treatment always indicated: \ Endograft extension \ Cuffs \ Balloon moulding \ Endoanchors \ Surgical explantation \ Type 2 endoleak Retrograde flow from side branchesa From intercostal, lumbar, inferior mesenteric and often cease spontaneously 50% in 1 year Treatment: \ Watchful waiting \ If significant aneurysm sac expansion or false lumen expansion present – become type I \ Embolisation of side branch \ Embolisation of sac (Onyx) \ Type 3 endoleak Disconnection of endograft components or tears in the endograft Treatment always indicated: \ Graft relining / additional overlapping graft \ Surgical explantation and repair Type 4 endoleak Graft porosity Rare with new devices. Usually no treatment required \ Type 5 endoleak Ongoing aneurysm sac expansion in the absence of any other demonstrable endoleak Explantation or relining of the whole stent-graft \ Device migration Can result in endoleaks \ Device dislocation Treatment: \ Device kinking \ Relining with additional stent-grafts/stents \ Surgical explantation \ Graft occlusion Treatment: \ Thrombolysis and perhaps balloon angioplasty and/or graft-stent relining \ Surgical bypass for limb occlusion or rarely complete surgical revision \ Graft infection Treatment: \ Long-term antibiotics \ Surgical explantation Exam 2016 part 2 Angio EVAR EVAR “Treat, No treat, Treat, No treat, Treat for endoleak types from 1-5” Device migration can result in limb kinking and occlusion, thrombus formation, distal embolization Seen in Type I and Type III endoleaks Treated by additional stent-graft insertion If this fails, then surgical repair Device kinking and device dislocation can happen without migration due to changes in vessel Most common is Type II leak Abdominal biopsy complications: Hemorrhage Pancreatitis after pancreatic biopsy. Causes of acute upper GI blaeeding: Ulcer Gastritis Lower bleeding: 80% colonic, right colon ->transverse->sigmoid->rectum. Diverticulosis->angiodysplasia CTA sensitivity 95% (bleeding rate 0.5-1 ml/min). Use of CO2 gas help to identify the bleeding. Object of embolization in gastrointestinal bleeding is to decrease arterial pressure and flow sufficiently to allow hemostasis without creating tissue infarction. In general coils, pieces of Gelfoam, metamorphics (e.g., glue), or particles are used. CHEMOEMBOLIZATION = TACE Digital spot image after embolization showing retained oil in the tumor (arrow) and shunting into the adjacent portal branches (arrowhead), an angiographic endpoint for the procedure. Liver gets blood from portal vein and hepatic artery Malignant tumors get most blood supply from hepatic artery Reduced systemic side effects of chemotherapy Trans arterial chemoembolization TACE can treat both HCC and metastases Most suitable are patients with HCC with preserved liver function and ECOG performance status 0-1 with no extrahepatic disease Also, in advanced metastatic disease to prolong life, if there is no extrahepatic or stable extrahepatic disease Also used initially to reduce tumor bulk to make tumor respectable Contraindications are little liver reserve: with over 50-75% of liver replaced by tumor advanced cirrhosis liver failure advanced or progressive extrahepatic disease Relative contraindications: Child-Pugh Class C Hepatic encephalopathy Active GI bleeding Refractory ascites TIPS Bilirubin>5mg/dl Complications: overall rate 4% Post-embolization syndrome PES Within 12h up to 7 days Nausea, vomiting, fever, malaise – no need to treat if present later Prevented and ameliorated by analgesia, antiemetics, antipyretics and intravenous fluids during and immediately after the procedure Hepatic failure due to infarction, abscess, biliary necrosis with biliary structure, tumor rupture, nontarget embolization especially of gallbladder wall Assess tumor response after 6 weeks with CT or MRI RADIOEMBOLIZATION = SIRT Selective intra-arterial radiotherapy SIRT or intra-arterial brachytherapy, radioembolization Allows to deliver higher radiation doses than external beam radiotherapy with minimized radiation dose to normal tissue Suitable for: Unresectable lesion Lack of fitness for transplant Lesion unsuitable for thermal ablation Failed conventional chemotherapy Uses 90Y HCC has significant pulmonary shunting Need to determine lung-shunting fraction Use technetium 99 macroalbumin aggregate albumin (99TC-MAA) Diagnostic mesenteric angiography performed before SIRT because: 50% of population has aberrant hepatic arteries 15% has aberrant hepatic arteries supplying GI tract Use proximal coils to embolize arteries to normal tissue – this is to prevent later non-target tissue embolization No ischemia due to collateral supply to the GI tract Proximal coils protect the bowel from embolization 90Y so that delivery is only to the tumor DDx from embolization of GI bleed – distally distal coils are used to avoid ischemia Non-target tissue embolization in SIRT is greater problem than with TACE chemoembolization as 90Y causes ischemia and radiation injury More effective than chemoembolization to downstage HCC but has more side effects due to radiation One lobe treated at one time with 4 weeks between lobar treatments Post-radioembolization syndrome similar to PES, conservative management Radiation hepatitis 0%-4% Cholecystitis 1% Gastrointestinal ulceration <5% Postembolization syndrome requiring extended stay or readmission Pain, fatigue, nausea 20% Biliary (focal dilation, biloma) Other complications: Biliary structure Radiation cystitis Portal HTN Radiation pneumonitis GI complications from non-target Hepatic dysfunction Wait 6-9 months between radiotherapy and tumor resection to allow full response PTC / PTD / Percutaneous Transhepatic Drainage indications Benign biliary strictures Usually benign strictures after laparoscopic cholecystectomy but also Posthepatic transplant ischemic stricture Biliary atresia Choledochal cysts SC sclerosing cholangitis Transhepatic drainage can be performed in benign strictures or gallstones to: Drain an obstructed infected system not amenable to ERCP endoscopic drainage ERCP unsuitable for intrahepatic gallstones Dilate benign strictures, often iatrogenic secondary to laparoscopic cholecystectomy, biliary-enteric anastomotic strictures/choledocho-jejunostomy (including post-hepatic transplant) or sclerosing cholangitis Post-anastomosis ERCP usually not successful due Roux loop or Billroth II gastric anastomosis Percutaneous fluoroscopy-guided dilation of the stricture and/or stone extraction Treat intrahepatic or ductal calculi At least 2 weeks of biliary drainage with catheter across the stricture Biliary obstruction due to CBD calculi First-line management is ERCP PTC if ERCP unsuccessful or intrahepatic calculi Cause small but significant incidence of pancreatitis Axial computed tomography scan of the abdominal aorta A, Image without contrast abdominal aortic aneurysm. The wall of the aneurysm is identified by the calcification in the intimal layer (arrow). The patency of the aneurysm cannot be determined from this image, but mural thrombus containing calcium (arrowhead) is present. B, Contrast-enhanced image at a similar level shows the aortic lumen. The mural thrombus is lower in density than the blood. Without the precontrast study the calcified areas in the thrombus ould be misinterpreted as contrast. Nongated and gated CTA of the thoracic aorta in a patient presenting with recurrent embolic strokes This patient had a mural aortic thrombus secondary to a hypercoagulable condition. Chronically occluded superficial femoral artery (SFA). Focal stenosis in the popliteal artery (arrow). B, Using progressively larger coaxial catheters, the lesion was dilate Stent-graft exclusion of an abdominal aortic aneurysm. A, Computed tomography (CT) scan before bifurcated stent-graft placement shows a patent aneurysm. B, CT scan at the same level 24 hours after stent-graft insertion. The lumen of the aneurysm is thrombosed. Note the air bubble (arrow) in the excluded aneurysm sac, a common early finding. C, CT scan 1 year later shows dramatic decrease in the diameter of the aneurysm (arrow). Normal shoulder anatomy on radiography. A, AP view in external rotation in an adult shows the greater tuberosity (short white arrow), glenoid rim (short black arrows), bicipital groove (black arrowheads), and acromioclavicular joint (long white arrow). B, AP view in internal rotation in a child shows glenoid rim (arrowheads), lesser tuberosity (arrow) and acromion (acr), distal clavicle (clv), and coracoid process (cor). Rotator cuff partial-thickness tears. A, Oblique coronal fat-suppressed T2-weighted image shows small partial-thickness undersurface tear (arrows). B, Extensive partial-thickness supraspinatus undersurface tear (arrows). Coronal T2-weighted MR arthrogram shows extensive partial thickness undersurface tear with only a thin layer of intact tendon (arrowheads). Note that there is no muscle retraction. The subacromial bursal fluid was due to a minute perforation of the infraspinatus (not shown). Rotator Cuff Tear Most frequent cause: Chronic impingement Other causes: Rheumatoid arthritis (pannus), acute injury Most frequent site: Supraspinatus anterior insertion onto the greater tuberosity Less frequent: Infraspinatus, subscapularis Confusing terminology: “Complete tear” means rupture of entire tendon to some but only a probe-patent perforation to others. Full-thickness tear: Bright T2 signal/low echogenicity across full thickness of tendon. Increased fluid in subacromial bursa. Look for tendon retraction. Chronic complete tear: Retraction, muscle atrophy Partial tear: Bright T2 signal/low echogenicity in tendon does not cross full thickness of tendon. May be upper (bursal), lower (humeral or articular), or intrasubstance. Rotator cuff tear Mostly supraspinatus anterior insertion On US: hypoechogenic On MRI: hyperintense T2 from fluid or granulation tissue DDx for labral tear need arthrography Chronically high-riding humeral head subluxation on XR is diagnostic Retraction >3-4cm has poor prognosis for surgical repair Shoulder dislocation Labral tear Labrum is hypointense on all MRI sequences Use MR arthrography, superior to MRI showing contrast flow into the tear Some are not visible on any imaging ABER position –. Anterior periosteal sleeve avulsion. Medially displaced Perthes. (inferior glenohumeral ligament) GLAD - glenolabral articular distribution. Buckle handle configuration SLAP tear has superolateral to inferomedial orientation while DDx sub labral recess is superomedial Can have suture anchors and tacks. Labral tear with periosteal striping - Perthes lesion. Superior labral anterior and posterior (SLAP) tears. Type 4 (bucket handle) SLAP tear. Axial fat-suppressed T1-weighted MR arthrogram image. Note the retracted biceps labral complex (between short arrows) and only contrast where the biceps long head normally attaches to the glenoid (arrowhead). The partially detached labrum (long arrows) connects the avulsed biceps labral complex to the glenoid in a bucket handle configuration. Bankart fractures in different patients. A, Radiograph shows a subtle fracture fragment inferior to the glenoid (arrows). B, CT shows anterior inferior glenoid fracture (arrowhead). C, Axial fat-suppressed T1-weighted MR arthrogram image shows Bankart fracture (arrow) with large medially displaced fragment (arrowhead). Hill-Sachs lesions A, AP radiograph in internal rotation shows a notchlike defect in the posterosuperior humeral head B, Grashey view shows a Hill-Sachs lesion (arrowheads). C, Coronally reformatted CT image shows similar defect (arrows). D, Axial T1-weighted MR arthrogram shows notchlike defect. Note that the Hill-Sachs lesion is seen at the level of the base of the coracoid process. More inferior notched contours are developmental in nature and should not be confused with a Hill-Sachs lesion. C, Coracoid process. Multiple Myeloma Most common appearance: Multiple punched-out lytic lesions (rare solitary leasion – plasmocytoma) May present as diffuse osteopenia, without focal lytic lesion Occasionally presents as a focal lytic expansile lesion (plasmacytoma) Radiographic skeletal series less sensitive than whole body magnetic resonance imaging. Plasmacytoma. A and B, Solitary large lytic lesion of the iliac wing. (A) and CT scan (B) show a large, sharply marginated, purely lytic lesion with cortical breakthrough. This is a typical appearance of plasmacytoma. C, Sagittal T2-weighted MR image of sacral plasmacytoma (arrows) in a different patient. This appearance is not specific, but this is a common presentation of myeloma Metastases Purely lytic: Lung most frequent, followed by kidney, breast, thyroid, gastrointestinal (GI), neuroblastoma. Blastic: Prostate, breast, bladder, GI (adenocarcinoma and carcinoid), lung (usually small cell), medulloblastoma. Mixed lytic and blastic: Breast, lung, prostate, bladder, and neuroblastoma. Therapy or radiation necrosis can change the lesion density (e.g., lytic metastases heal to more normal density). Most metastases occur where red bone marrow is found; therefore 80% of metastases are located in the axial skeleton (ribs, pelvis, vertebrae, and skull). A lesser trochanter avulsion fracture in an adult should be considered pathologic until proved otherwise in patients with known breast cancer, a solitary sternal lesion is rare but, if present, has an 80% probability of being caused by metastatic disease. Finally, the presence of a transverse fracture in a long bone, especially without significant prior trauma, should alert the radiologist to the possibility a pathologic fracture Ankylosing spondylitis (AS), sacroiliac (SI) joints. A, symmetric findings of slight widening of the SI joints, sclerosis, and erosions that are more extensive in the inferior (synovial) portion of the joints (arrows) B, T1-weighted coronal MR w shows bilateral hypointensity along the SI joints, with widening and erosions, more prominent on the right than the eft (arrows). C, Fat-saturated T2-weighted axial imaging of the same patient shows marrow edema on both sides of the SI joints, as well as bilateral erosions (arrows). D, End-stage complete SI joint fusion. AP radiograph shows SI joints that are completely fused bilaterally. ,Coronal CT of the SI joints in the confirms signs of AS, with joint space widening, erosions, and sclerosis. \ Psoriatic Arthritis Most cases: Asymmetric erosive arthropathy, with superimposed bone productive changes Five patterns: Oligoarthritic (sausage digit) Polyarthritis: DIP nore then PIP and MCP joints. Symmetric type like RA Arthritis mutilans (deforming type, pencil-in-cup) Spondyloarthropathy (bilateral, asymmetric sacroiliitis, bulky asymmetric osteophytes usually starting at the thoracolumbar junction, noncontiguous) Bone density can be normal Distal phalanges: Tuft resorption or reactive sclerosis (“ivory phalanx”) Arthropathy may precede skin changes—up to 20% of cases Psoriatic arthritis, polyarthritis pattern. PA view of the hand demonstrating predominantly distal interphalangeal (DIP) joint disease, with fusion at the fourth DIP joint (arrow). Note also the subtle periostitis at the proximal phalanges of the third and fourth digits (arrowheads). Fusion and periostitis are hallmarks of psoriatic arthritis. Also note the small erosions at the third DIP joint Psoriatic arthritis, arthritis mutilans pattern. A – destruction in DIP 1,2,3 – Pencil in cup appearance. B - only the “pencil-in-cup” of the third and fourth proximal interphalangeal joints (arrows) but also the new bone production (“periostitis”) at the distal phalanx of the great toe (arrowheads) Scaphoid fractrure Commonest carpal bone usually occult on XR In children - more common on distal third portion In adults – more common in waist portion with higher risk of AVN of proximal portion More risk of non-union, delayed union, AVN the more proximal the fracture is Similar distribution in to talar dome, head of femur Mild proximal pole sclerosis does not indicate AVN or poor prognosis Avascular necrosis necrosis of the proximal pole T1 hypointense. SNAC – chromic ununited fracture of the scapjoid wrist with avascular necrosis of the proximal pole, dorsal tilt of the lunate bone. Scaphoid fracture complications. 1 – NON union SNAP (scaphoid nonunion advanced collapse). b- Delayed union, successfully treated with bone grafting. the graft fragments (arrows) and the graft donor site in the distal radius (arrowhead). C, Humpback deformity. Oblique coronal CT image aligned with the scaphoid shows dorsal tilt of the proximal fragment (black line) and volar tilt of the distal fragment (white line), resulting in the “humpback” deformity. NOF – Non ossifying fibrous cortical dysplasia Very common, often found incidentally in pediatric radiographs, especially around knee. Does not require further work up. Bubbly lytic lesion with sclerotic margins Cortical metadiaphyseal lesion Larger lesions may present with pathologic fracture Most common natural evolution is to be replaced by bone (“heal”) over a few years with mild residual sclerosis NOF > 2 cm, FCD <2 (fibrous cortical defect) Children > 2 years old. Knee, ankle Posterior femoral metaphysis knee Supracondylar fracture displaced anterior and posterior fat pads (white arrowheads) and posterior displacement of the capitellar growth center relative to the anterior humeral line B, AP view shows the lateral aspect of the fracture line. Humeral supracondylar fracture Commonest pediatric elbow fracture, fall on outstretched hands. Hyperextensiom force -> transverse fracture of the humerus condyl. Posterior fat pad sign. Posterior displacement of the capitalum. Lateral condyle fracture Second common in children Lateral fall with arm on the side. Avulsion type fracture (complete or incomplete) Incomplete: don’t extend physis, may involve lateral condyle SALTE-HARRIS 4. (stable, casting) Complete fracture – distally to the articular surface. Extension type more common with posterior displacement of distal fracture fragment Complications: Nerve entrapment Malunion Osteochondral defects AVN A, Salter-Harris IV fracture. AP radiograph shows the fracture extending through the distal lateral metaphysis (arrowhead) and the capitellar growth center (arrow),. B, Displaced complete fracture. Note the fracture (arrows) proximal to the capitellar physis (arrowhead). The fragment is displaced laterally. The fracture extended distally and medially through unossified trochlear cartilage C, Complete fracture. The fragment is displaced laterally and rotated. Note the small metaphyseal fragment (arrowhead) and the capitellar growth center (long arrow). Summary of elbow fractures in children Fat pad sign is usually present, but is less sensitive and specific for fracture than in adults SUPRACONDYLAR FRACTURE (65%) Fall on an outstretched hand causes elbow hyperextension Abnormal anterior humeral line MEDIAL EPICONDYLAR AVULSION (10%) Fall on an outstretched hand causes valgus stress Possible medial condylar entrapment—don’t miss it as fuses in weeks with deformity LATERAL CONDYLAR FRACTURE (15%) Lateral fall with arm at side causes varus stress across elbow May be incomplete, involving only part of the physis Testicular torsion Peak peripubertal boys Smaller peak in infancy. Normally intra-tuniaically In some group – tunica vaginalis (bell clapper demormity) Testicular salvage rates are closely related to time to diagnosis; salvage rates of 80% in the first 6 hours drop to 20% if surgery is delayed for more than 24 hours Torsion shows ipsilateral increased echogenicity with absence of intratesticular flow. Adrenal adenoma CT 10 HU – lipid-rivh adenoma -. No work up Adenomas enhance rapidly after contrast administration and rapid washout of contrast medium—a phenomenon termed ‘contrast medium washout’. Malignant lesions and phaeochromocytomas enhance rapidly but demonstrate a slower washout of contrast medium.  Adenomas which contain intracellular lipid lose SI on out-of-phase images compared to in-phase images, whereas malignant lesions and phaeochromocytomas which lack intracellular lipid remain unchanged. MRI: After gadolinium enhancement, 90% of adenomas demonstrate homogeneous or ring enhancement while 60% of malignant masses have heterogeneous enhancement. On the out-of-phase image, both drop significant visual signal intensity Ovarian torsion Rotation on vascular pedic Reproductive age, young Associated with cyst or ovarian dermoid tumor Most common finding is ovarian enlargement >7cm Smaller ovary excludes this On US /on MRI: Swirl sign of ovarian pedicle / whirlpool sign Ascites Follicles displaced peripherally Beaking of the ovarian lesion Abnormal location of ovary – anterior or posterior to uterus Deviation of uterus to affected side As there is dual blood supply to the ovary, a lack of Doppler signal is a much less reliable sign than in testicular torsion. Ovarian Torsion. (A) Sagittal and (B) axial T 2 weighted magnetic resonance imaging of an extreme example of a torted ovarian fibroma with cystic degeneration. The classical features of the swirl of the torted pedicle (black arrow) and the ‘beaking’ of the ovarian lesion (white arrows) are well demonstrated within the high T 2 free fluid within the abdomen. B , Bladder; U , uterus. Duplex Kidneys Lower moiety – insertion superior and lateral - risk of VUR. Upper moiety – insertion distal and medial - ureterocele, dysplasia, obstruction. Upper moiety is usually dilated, particularly when associated with a ureterocoele or ectopic ureteric insertion, or may be atrophic. Uretrocele. Pelviureteric Junction Obstruction 40% cause of renal tract dilatation. Antenatal, postnatal US. US 7 days after birth. 7-10 mm. Prune-Belly Syndrome The combination of absence/hypoplasia of the abdominal wall musculature, UTD and bilateral undescended testes is known as ‘prune-belly syndrome’, or abdominal musculature deficiency syndrome Posterior Urethral Valves Congenital urethral obstruction, Boys with urosepsis. Renal insufficiency. Pulmonary hypoplasia – respiratory distress. Urethral Stricture Male 75% - congenital in bulbous urethra. Traumatic – bulbar. Pelvia trauma – membranous. Haematocolpos. Sagittal ultrasound image of thickened endometrium with spill of blood into the obstructed, distended vagina lying behind the normal bladder. Cryptorchidism 4% full term 30% preterm newborns. Unilateral testicular agenesis is associated with ipsilateral renal agenesis. Early diagnosis and treatmen prevent infertility and malignancy. US has estimated sensitivity and specificity of around 45 and 80% MRI mor sensitive – testicles hypoplastic T 2 low. Renal tract calcifications / nephrocalcinosis / renal calculi / urolithiasis Nephrocalcinosis is the deposition of calcium salts and commonly incidental finding Most nephrocalcinosis is medullary 95% and generally less severe, caused by metabolic dysfunction Causes of medullary nephrocalcinosis Medullary sponge kidney Hyperparathyroidism Hypervitaminosis D Renal tubular acidosis Beta-thalassemia Loop diuretics Sarcoidosis Primary hyperoxaluria “Oxalosis” (DDx also causes cortical nephrocalcinosis) More likely to cause nephrolithiasis as stones are closer to the collecting system Causes of cortical nephrocalcinosis Acute cortical necrosis Chronic glomerulonephritis Allograft rejection Alport syndrome Primary hyperoxaluria “Oxalosis” More severe, cortical disease US and CT better than AXR for nephrocalcinosis especially for less severe disease Note this is different than diagnosis of renal calculi – AXR better than US On US: hyperechoic renal parenchyma with posterior shadowing On AXR: stippled calcification Does cause papillary necrosis Nephrolithiasis refers to the formation of stones in the collecting systems Around 8% of patients with hematuria have nephrolithiasis 95% of renal colics have hematuria Calcium stones (calcium oxalate and calcium phosphate) 95%: radio-opaque Due to low fluid intake, hyperthyroidism, medullary sponge kidney Struvite stones (magnesium ammonium sulphate): radio-opaque Due to high urinary pH, infection (Klesbsiella, Proteus, Pseudonomas which are urease-producing) Form staghorn calculi Urate stones (uric acid): radio-opaque but less than calcium (p. 788), minority radiolucent Due to: high urine acidity in hot, dry climates, high BMI, diabetes, gout Use dual-energy CT to differentiate urate from non-urate calculi (material decomposition) Cystine stones: lower density or minority radiolucent Due to: metabolism disorder cystinuria (stones in childhood “cystine”) Xanthine stones: radiolucent Indinavir stones (from protease inhibitors), mucoid matrix stones are hypoattenuating on CT “Gays are exception” Primary hyperoxaluria causes both cortical and medullary nephrocalcinosis Drug-related stones: indinavir, acyclovir, sulfadiazine Xanthogranulomatous pyelonephritis Host response to granulomatous inflammatory process More in middle-aged women, diabetics DM E. coli, P. mirabilis Can occur with or cause: TCC Hematuria Retroperitoneal hemorrhage Renal vein thrombosis RVT Psoas abscess Cutaneous fistula or colonic fistula Extends into perirenal fascia, obscures kidney borders Starts from renal pelvis “starts and finishes in pelvis – TCC” Associated with renal pelvic stones / staghorn calculus – renal pelvis involved initially On AXR: staghorn calculus “Staghorn – Xanthogranulomatous” On US: Hypoechoic masses with internal echoes replace kidney parenchyma Dilated kidney with stones Stenosis of renal pelvis On CT: important to visualize borders and extra-renal disease before surgery Non-functioning enlarged kidney Central calculus Only 10% acalculous Expanded calyxes and contracted renal pelvis Fat stranding Hypodense kidney due to inflammatory infiltrate and not fluid Material inside it usually does not enhance On MRI: T1 hyperintense due to xanthine and fat T2 isointense or hypointense solid component to kidney T1 hypointense fluid and pus T2 hyperintense fluid and pus Renal AML / renal angiomyolipoma Fat, smooth muscle, abnormal blood vessel Presence of fat is diagnostic (-15HU or -20HU) More in women in 40-50 years “They can bleed and women bleed” Drop of signal on out-of-phase MRI due to macroscopic fat / intracytoplasmic lipid Bilateral and occur earlier in tuberous sclerosis Also rarely associated with: ADPKD NF neurofibromatosis Hemorrhage especially in lesions >4cm Fat-poor AML: avid enhancement On US: hyperechogenic even more than sinus fat, posterior shadowing Variable appearance, lipid-poor AML is not so hyperechoic RCC <3cm is also hyperechoic so cannot make diagnosis DDx RCC usually does not have posterior shadow On MRI: lipid-poor AML is hypointense on T2, use chemical shifting imaging Lipid-poor looks like DDx RCC On angiography: multiple aneurysms with onion layer appearance Prostatic artery embolization (PAE) Technically demanding due to the size of the vessels, tortuosity and anatomical variation Failure rates of up to 30% are reported. Advantages over surgery include a lack of incontinence and preserved sexual function. Ovarian vein embolisation Right common femoral vein Right internal jugular vein approach. liquids, sclerosants, Gelfoam, coils and vascular plugs to embolise both ovarian vein Varicocele Pampiniform plexus dilated, tortuous veins Idiopathic or secondary Associated with infertility >3 mm Superior and posterior to the testis DDx hydrocele is anterior and lateral to testis. Idiopathic are left sides (drain into left renal vein) Isolated right sided varicocele suspicious for intraabdominal mass. Cannot always demonstrate spontaneous flow Maneuvers to demonstrate flow: cough, inhale, Valsalva Treatment dilemmas as 20-80% of fertile men have subclinical varicocele Internal spermatic venography is not used anymore to diagnose but can be used for venous mapping for embolotherapy. Thyroid malignancy Signs of thyroid malignancy: Microcalcification. Hypoechoic lesion Peripheral calcifications Taller than wider. Lobulated border. Signs of benign lesion: Simple cyst Spongy Comet tail artefact. Most 90% are differentiated carcinomas, most 80% papillary thyroid carcinoma and rest follicular Rare anaplastic thyroid carcinoma (bad prognosis, 95% mortality, hypoechoic sold mass with coarse calcification). Nodules are very common, risk of malignancy only in 2-4%. 80% of patients – thyroid hyperplasia Signs of hyperplasia: cystic component, internal septations, thick walls, solid or subsolid nodules. Diffuse cystic lesions give sponge appearance, hypervascular. Crystals with comet tail artefact. Benign follicular adenomas 10% of follicular nodules, may cause hyperparathyroidism. Solid, homogeneus’ well defined with a thin hypoechoic halo. Follicular cancer 10% of malignancy women after 60. 80% minimaly invasine, 20% invasive. Hematogenous spread: bone, brain, lung, liver. Neck – very rare. On US: Variable echogenicity Well-defined Hypoechoic halo. Both US and FNA cannot tell benign from malignant – need histology Treated by lobectomy Papillary cancer: 75% of thyroid cancer (most common). survival rate of 90-95% within 20 years of diagnosis. Lymphatic dissemination, occult cervical nodes. Microcalcifications (calcius depositions in psammoma bodies). this increases the chance that the finding will be malignant Medullary 3s common, 5% Parafollicular cells (secrete calcitonin), tumor marker.agressiv do not response to chenio or radiotherapy. Ass with MEN 2. May have calcification, very vascular. Hashimoto Thyroiditis An autoimmune disease is the common cause of hypothyroidism in developed countries. Ages 40-60, more in women associated with thyroid lymphoma. Associated with other autoimmune diseases. The appearance of the gland in Hashimoto's normal size/enlarged hypoechoic. Replacement of the homogeneous tissue for heterogeneous coarse tissue. Often a extremely vascular gland. Predominantly central reactive lymphadenopathy below the gland is common. In the advanced-final stage the gland is atrophic. Can have solid hypoechoic nodule Even more hypervascular than DDx Graves’ disease Graves’ disease Most common cause of hyperthyroidism. Autoimmune disease. W>m Diagnosis by blood test. US: enlarged, hyper vascular PARATHYROID US: Zuckerkandl’s tubercle can mimic it but part of normal thyroid with separated tissue. Parathyroid adenoma It is usually a single hypoechoic, hypervascular, homogeneous mass of various sizes, solid (sometimes so hypo that it sometimes simulates a cyst). The structure is often oval parallel to the course of the neck (higher than wide). Commonest cause of hyperparathyroidism The common locations are lateral to the trachea and esophagus, medial to the CCA and postero-inferior to the thyroid. 50% half are ectopic: retro tracheal - common, the carotid sheath or within the thyroid gland in the back. superior mediastinum anterior to the thymus - a challenging location for sonographic identification. In the minority of cases there will be a cystic component and even less common is a completely cystic adenoma. BOX 10-2 Characteristics of Parathyroid Adenomas Solid Hypoechoic Oval Hypervascular (variably detected) Posterior to thyroid Medial to the carotid artery SALIVARY GLANDS US Most tumors of the salivary glands are in the parotid gland (80%) and 20% submandibular Parotid gland - up to 85% benign tumors. Submandibular gland - about 50% benign and 50% malignant Sublingual gland - 30% benign and 70% malignant Parotid pleomorphic adenoma A benign tumor that accounts for 70% most of tumors in the parotid (50% in the submandibular) usually develops from a superficial lobe. cancerous transformation in 10% of cases Hypervascular Sialolithiasis The most common pathology in the salivary glands 80% will be in the submandibular duct and 20% in the parotid duct In 50% of the cases of stones we will see inflammatory changes in the gland Sjögren / Sjogren syndrome Distinctive clinic of dry mouth, dry eyes, autoimmune disease, more in women. Increased hypervascularity and scattered hypoechoic nodules report. Mostly involves parotid gland. Link to MALT (from Grainger) Branchial cleft cysts Most 90% of branchial cleft cysts arise from the second branchial cleft. They are typically located in the submandibular area anterior to the sternocleidomastoid muscle, posterior to the submandibular gland or lateral to submandibular gland, and lateral to the carotid artery. Aneurysmal SAH / Brain aneurysms Saccular, fusiform, dissecting Majority are saccular aneurysms Arise from arterial bifurcation Giant aneurysm >2.5cm – 5% PCom aneurysm – compression of cisternal segment of CN III Note that CN III passes between SCA and PCA ACom aneurysm – causes SAH + intraparenchymal hemorrhage in inferior temporal lobe Clot in septum pellucidum and extending into frontal lobe is pathognomonic with ACom PICA aneurysm – brainstem MCA aneurysm – bleed into Sylvian fissure, clot in temporal lobe ACA aneurysm of pericallosal branches uncommon 90% most arise from anterior circulation / carotid circulation ACom 1/3 PCom 1/3 – ICA is origin of PCom MCA 20% Tip of basilar artery 5% PICA 20% have multiple aneurysms Disperses quickly when bleeds, hard to tell origin Treat anterior circulation aneurysm if >7mm - if smaller, no benefit unless previous history Always treat posterior circulation aneurysm DSA is gold standard imaging for intracranial vascular abnormalities. CTA – initial. MRA in non-acute setting. DAI Diffuse axonal injury Rapid deceleration in RTA Stretching and shearing of axons – usually found in white matter Subcortical and deep white mater – grade I Corpus callosum – grade II Brainstem – grade III On CT: only seen if hemorrhage accompanies it Hemorrhage in deep white matter and corpus callosum – more severe injury – possible DAI Can have clinic without CT findings – prompt MRI On MRI: most sensitive sequence is GRE – T2* or SWI – to detect microbleeds CT A,B: Subcortical white matter hemorrhage -left frontotemporal lobe. SWI: C,D – DIA left cerebrum. (grade 1) UPPER ROW – SWI: right frontal parasagittal line: GRADE 1: A-white matter, thalamus © GRADE 2: B – corpus colosseum. GRADE 3: ,D brainstem. Lower row is T2. Deep neck spaces parapharyngeal space (PPS), parotid space (PS) retropharyngeal space (RPS) danger space (DS), masticator space (MS) carotid space (CS), pharyngeal mucosal space (PMS) perivertebral space (PVS). Mandibular Osteosarcoma Carotid and vagal paragangliomas. Schwannoma. Axial T 2 magnetic resonance image. The nasopharyngeal tumour (white star) has extended posteriorly (interrupted white line) and on the right laterally to invade the perivertebral space and parapharyngeal space. Note the remaining partially invaded left prevertebral muscle medial to the ICA (white arrow) . Oropharynx Tonsillar Squamous Cell Carcinoma. Axial T 2 magnetic resonance image of left tonsillar squamous cell carcinoma ( SCC ). Note the left tonsillar SCC (interrupted white line) invading the following areas: 1, posterior pharyngeal wall, 2 , RPS, 3 , parapharyngeal space abutting the medial pterygoid muscle, 4 , tongue. Parapharyngeal space PPS Fat from skull base to submandibular space Direction of displacement important to know where lesions is from Parotid space PS Contain parotid gland, Lymph nodes. Fascial nerve. Retromandibular vein. External carotid enclosed superficial deep cervical fascia. *Pleomorphic adenoma Retropharyngeal space RPS and danger space DS From skull base to T4 posterior to pharynx and anterior to prevertebral muscles Cannot tell DS on imaging Fatty density line – check if preserved Pathology of RPS usually unilateral – lymph nodes from skull base to hyoid bone (suprahyoid lymph nodes) Infection can spread to mediastinum Try to distinguish abscess with mass effect and enhancement from simple edema Important region to review when staging nasopharyngeal, oropharyngeal, sinonasal and hypopharyngeal malignancy Commonly involved in malignancy with involvement of lymph node Less commonly direct spread of posterior pharyngeal wall Malignancy *Retropharyngeal lymph nodes. Masticator space MS: Contain mastication muscles, trigeminal nerve 3. Mandibula -soft-tissue osteomas. (Gardner syndrome) Carotid space CS Contains arteries, IJV, sympathetic plexus, CN IX-XII in suprahyoid neck and CN X in infrahyoid neck - vagus Carotid artery dissection – Extracranial internal carotid artery - m.c. MRI T1 fat sat – best, intramural hematoma high. Glomus tumors/paragangliomas of carotid and vagus Salt and pepper appearance Vascular In carotid bifurcation Splay the ICA and ECA – spreads them apart 10% rule – 10% are bilateral Can be multiple Review jugular foramen for spread – permeative erosion Schwannoma Well-defined, homogeneous enhancement Fusiform shaped Can have cystic change. If vascular cannot dell from DDx paraganglioma but if extend into jugular foramen they remodel and expand it (like they do to IAC in the ear) Pharyngeal mucosal space PMS PMS include the mucosa of the nasopharynx and oropharynx, lymphatic tissue of Waldeyer ring, Nasopharynx Skull base, C1. eustachian tube opening and posteriorly the fossa of Rosenmüller. NPC usually arises in the lateral pharyngeal recess (of Rosenmüller) – most common nasopharyngeal malignancy. Nodal metastasis – common. Association with EBV. NPC mts : liver, bones, head and neck. Prevertebral space Common are abscess, metastases When lesions arise in prevertebral part of this space, they displace prevertebral muscles anteriorly DDx retropharyngeal space mass pushes muscles posteriorly Most common – tonsillar/peritonsillar abscess. May be complicated by spread to adjacent spaces, commonly parapharyngeal, masticator and submandibular spaces.   All oropharyngeal malignancy is SCC; the commonest site is the faucial tonsil and anterior tonsillar pillar Adenoid cystic carcinoma. Arise in the minor salivary glands of the subglottic and should be considered in the differential of a subglottic or tracheal mass. Parathyroid Adenoma. Arterially enhancing lesion abutting the inferior pole of the right lobe of the thyroid gland. Pineal region germinoma Most common CNS GNT then non-secreting teratoma Found in midline, pineal region or suprasellar region Malignant tumor but respond well to chemotherapy On CT: hyperdense solid mass within posterior 3rd ventricle, enhance vividly and homogeneously Diagnosis made by fetoprotein and chronic gonadotrophin in the CSF. Young men. MRI: T1+ enhancement. DWI restriction. Hugh choline. Low NAA. Teratoma inhomogeneous on CT and MRI, reflecting fat content and calcification. Pineal germ cell tumour. Contrast-enhanced T 1 (A) shows an enhancing pineal region tumor compressing the third ventricle, which contains areas of susceptibility artefact (signal dropout) on T 2 * (B) and avid tracer uptake on a choline positron emission tomography (C). Dysembrioplastic neuroepithelial tumors CHAPTER ADULTS DNT DNET (WHO grade I) Presents with complex partial seizures in adults younger than 20 years Benign glioneuronal neoplasm. Supratentorial cortex, coplex partial seizures. CT hypo, MRI: An axial T 2 (A) and a sagittal T 1 (B) showing a T 1 -hypointense and T 2 -hyperintense cortically based tumor with a ‘bubbly’ appearance. Thinning and remodeling of the overlying bone is also demonstrated. Dysembryoplastic Neuroepithelial Tumours CHILDREN DNT is a WHO grade I benign tumour which classically presents with complex partial seizures in children and young adults younger than the age of 20. It is a cortically based lesion which may have associated foci of cortical dysplasia. On imaging it appears as a well-defined cortically based lesion with a characteristic ‘bubbly’ internal structure, minimal mass effect and no associated vasogenic oedema  On MRI they are hypointense on T 1 and have a hyperintense rim on FLAIR or proton density-weighted imaging ( Fig. 76.70 ). Most tumours do not enhance and, if present, enhancement is faint and patchy. Ependymoma Rare in adults, mostly children. Intraventricular, may be cerebral hemisphere tumors. 4d ventricle ependymomas from foramina Magendie and Lushka. Two peaks at 5 and 35 year. CT: well demarcated lobulated mass lesion,.50% with calcification. MRI: mixed intensity. T2 hyper, hypo on T1. Enhancement heterogeneous. Epidermoid, dermoid cysts Dermoid contain all skin elements, including fat, and appear therefore of very low density on CT and of high signal intensity on T 1 images. On CT, epidermoid cysts generally appear as well-circumscribed, lobulated, non-enhancing, homogeneously hypodense lesions (of similar density to CSF. On MRI, epidermoid cysts have signal intensity close to that of CSF on T 1 , T 2 and FLAIR images, which can make them difficult to distinguish from other cystic lesions such as arachnoid cysts. DWI - markedly hyperintense, indicating restricted diffusion. Flexion-compression and flexion-distraction injuries Sagittal T 2 weighted magnetic resonance imaging; there is compression of the anterior aspect of the vertebral body (arrowhead) and interspinous ligament disruption of the level above (arrow) , with disruption of the ligamentum flavum and high signal passing through the interspinous ligament. Flexion-compression fracture Loss of height in anterior aspect of vertebral body with intact posterior ligaments If the vertebral collapse is substantial, more suggestive of flexion-compression injury If it involves posterior vertebral wall, the posterior ligaments will be intact as this is a burst fracture. Flexion-distraction fracture Ruptures the posterior bony structures (minimal degree) and posterior ligaments – highly unstable If involves posterior bony elements it is a bony Chance fracture “distracted by chance” – heals better if PLL intact If soft-tissue Chance – on CT cannot discriminate from the simple DDx flexion-compression fracture with intact posterior ligaments Main clue is kyphosis – not hematoma or fat stranding With ligament rupture there is hemorrhage into epidural fat – dirty fat sign MRI still gold-standard Burst Fractures Axial compressive force through the spine. commonest thoracic and lumbar spinal fracture. Fracture affects anterior and posterior wall. Absent dirty fat sign -> ligaments are intact. Cushing Adrenal adenomas Hyperfunctioning ACTH-secreting adenomas. 2-7 cm. 95% hyperfunctioning, lipid rich. Contralateral normal or atrophic (low ACTH). 80-85% ACTH dependent, secondary to pituitary tumor. heterogeneous mass, surgically confirmed as an adrenocortical carcinoma (ACC) Prion Disease CJD: -50-60 decades. Sporadic Subacute dementia Myoclonus Motor disturbance. to Creutzfeldt–Jakob disease (CJD) , fluid-attenuated inversion recovery (FLAIR) images show mildly increased signal intensity in multiple areas of the neocortex, which are much more prominent on diffusion-weighted imaging (DWI) . Carbon Monoxide Intoxication. Bilateral globus pallidus necrosis. Lenticular nucleus, caudate. T1 low, T2 high DWI shows diffusion restriction in the basal ganglia Heavy Metal Poisoning accumulation of manganese and neuronal loss in the basal ganglia. MRI as bilateral hyperintensity on T 1 weighted sequences of the globus pallidus, which may extend to the cerebral peduncles  T 1 weighted magnetic resonance images of the brain in a patient with chronic liver failure. Observe the bilateral and symmetrical high T 1 signal-intensity change involving the globus pallidus and the anterior midbrain ( arrow in C). Fabry Disease Metabolic disorder. Axial T 2 -FLAIR- (A) and T 2 - (B) lacunar strokes involving the deep white matter, the right thalamus and the brainstem, associated with diffuse bilateral white matter hyperintensities. increased diameter of the basilar artery (arrows). Most prominent manifestations include cerebrovascular events, such as transient ischemic attacks and strokes, chronic cerebral vasculopathy, and vessel ectasia, especially in the posterior circulation. Increased basilar artery diameter. MELAS Stroke-like events, encephalopathy, seizures and myopathy. The diagnosis is based on the presence of lactic acid in the CSF. MRI demonstrates migrating cortico-subcortical T 2 hyperintensities, predominantly in the parietal, temporal and occipital lobes. The topography of the lesions does not correspond to a single vascular territory. After gadolinium injection, cortical and leptomeningeal contrast enhancement can be identified. DWI may show restricted or increased MELAS is an acronym for mitochondrial encephalopathy, lactic acidosis and stroke-like episodes. It is secondary to a mitochondrial DNA mutation. Wernicke Encephalopathy Vitamin B 1 (thiamine), MRI, bilateral and symmetrical hyperintensity on T 2 weighted sequences are evident at the level of the mamillary bodies, periaqueductal regions, medial thalami, third ventricular walls, pons, medulla and basal ganglia. Rarely, the cortex can be involved. The anatomical regions most frequently involved are the medial thalami and the periventricular regions of the third ventricle mamillary body hyperintensity.