2016-1.docx

Hepatic Adenoma primarily of hepatocytes, with no portal tracts or bile ducts and no bilirubin excretion; differentiate adenomas from FNHs by using hepatocyte-specific contrast agents. On CT, adenomas may be isointense with adjacent liver, or of slightly increased or decreased attenuation. Fat-suppr...

Hepatic Adenoma primarily of hepatocytes, with no portal tracts or bile ducts and no bilirubin excretion; differentiate adenomas from FNHs by using hepatocyte-specific contrast agents. On CT, adenomas may be isointense with adjacent liver, or of slightly increased or decreased attenuation. Fat-suppressed T 2 weighted image hyperintense masses. These appear isontense on in-phase gradient-echo imaging T1, hypervascular on arterial phase Telangiectatic Adenoma. On fat-suppressed T 2 weighted MRI, hyperintense rim, which is typical for this type of adenoma reflecting dilated sinusoids (peliosis components) within the mas Out-of-phase gradient-echo no fat within the lesion, while the liver is slightly steatotic and shows a subtle loss in signal when compared with the mass (B). The masses are both hypervascular on arterial phase T 1 weighted with a thin hypovascular rim ( arrowhead in C) and demonstrate persistent enhancement on the equilibrium phase (D). Biliary hamartoma CT often reveals their relatively cystic nature but, as the lesions may have a solid component. T2 MRCP Liver lesions with central scars FNH Hemangiomas Liver adenomas HCC Fibrolamellar carcinoma Focal Nodular Hyperplasia Women 20-50 years Multiple in 20% Vascular malformation Enlarges to hormone stimulation – COCP In FNH biliary elements not connected to biliary tree DDx from hepatic adenoma 50% central stellate fibrovascular scar – spoke wheel on US Differential diagnosis of liver central scar DDx HCC Hepatic adenoma Hemangioma Lacks true capsule – has fibrous pseudocapsule like DDx hepatic adenoma Very rare calcification, necrosis, hemorrhage Do not outgrow blood supply, DDx from hepatic adenoma does outgrow it On US: similar echogenicity to liver ON CT: can have mass effect displacing adjacent vessels avid enhancement in arterial phase – not central scar equilibrium and disappearance in portal phase and later large feeding vessels peripherally scar enhances on delayed phase On MRI: often hard to see on spin-echo low T1 (also central scar) high T2 (also central scar) T1 with hepatocyte-specific contrast like gadoxetic acid has avid enhancement with retention due to abnormal bile ducts DDx from hepatic adenoma – no avid enhancement, no retention Focal Nodular Hyperplasia (FNH) MRI. on fat-suppressed multishot T 2 weighted fast spin echo (A) unenhanced T 1 weighted (B) avid arterial phase enhancement (C), becoming isointense in the portal (D) and delayed phases (E). central scar is evident on some of the images (arrowhead) , which enhances on the delayed image (E). Gallbladder polyps Most often cholesterol Smal and multiple. Radioopaque only <10% seen on AXR Ultrasound is the investigation of first choice for diagnosing gallbladder calculi and cholecystitis. Gallbladder polyps are rarely significant when <5 mm and only require follow-up or consideration of cholecystectomy when >10 mm. Polyps 5–10 mm in size can be followed unless specific risk factors obtain (see text). CT and CEUS both can assist in diagnosis of cholecystitis, grading its severity and detecting potential complications. Adenomyomatosis is commonly mistaken for polyps or carcinoma and can be best diagnosed with US (including CEUS) and MRI. Pancreatic CF T 1 weighted innumerable cysts in both kidneys, the liver and the pancreas (arrows) ., multiple cysts (arrows) are shown at CT. 85% most have exocrine insufficiency with steatorrhea MPD obstruction – like in chronic pancreatitis (but no obstructing mass) Fatty replacement and dystrophic calcifications with cysts from duct obstruction Rely on clinical history for diagnosis. Von Hippel–Lindau Disease Autosomal dominant RCC Pheochromocytoma Retinal angiomatosis Hemangioblastoma cerebellum. TIPS hepatic portal vein branch (usually the right) and a hepatic vein. Indication: variceal bleeding -refractory. Refractory ascites. Hepatic hydrothorax. Portal hypertension. Complications: Cardiac failure. Encephalopathy 5 to 35%. Porto-systemic shunt – deliver the blood from the liver to stomach, esophagus, done when TIPS dose not work. Primary Sclerosing Stricture and dilatation. IBD on background.80% Multiple segments – intra/extrahepatic. Cholangitis (PSC) and Cholangiocarcinoma. Cholangiocarcinoma complicates about 10% of PSC. MRCP with contrast-enhanced T 1 acquisitions is more sensitive and specific for detecting Peritoneal carcinomatosis (PC) implantation of tumor deposits along the peritoneal surfaces of the diaphragm, liver and spleen results in smooth, nodular or plaque-like thickening and contrast enhancement of the parietal peritoneal lining Ovary (71%), stomach (17%) and colorectal (10%) cancers. Other causes: Peritoneum, including TB, peritoneal mesothelioma and peritoneal lymphomatosis. mimics such as splenosis, which can simulate peritoneal deposits. Calcification within peritoneal implants before chemotherapy suggests a potential ovarian (or gastric) primary lesion. irregular mass in parietal peritoneum. Deposit at the splenic hilum  Selenosis Mimicking Peritoneal Carcinomatosis. Contrast-enhanced T 1 weighted MR ‘line-type’ enhancement along the peritoneal surfaces Omental ‘Cake’ Infiltration (Peritoneal Carcinomatosis). Pseudomyxoma peritonei Peritoneal neoplasia due to a ruptured, benign or malignant mucin-producing tumor of the appendix, ovary and, occasionally, pancreas, stomach, colorectal or urachus. Low on CT, high on MRI. Ascites with septations. Scalloping of the visceral surface, liver, peritoneal implants. Lymphatic Dissemination dissemination of lymphoma to mesenteric lymph nodes. Confluent lymphomatous nodes may surround the mesenteric vessels, producing a ‘sandwich’ or ‘burger’-like appearance. Mesenteric Carcinoid CT - smoothly marginated enhancing mesenteric mass (white arrow) and an aggressive desmoplastic reaction retracting the affected ileum loops. PET - somatostatin-receptor scintigraphy with 111 In-octreotide. 40%–80% of gastrointestinal carcinoid tumors spread to the mesentery. Desmoplastic reaction - secondary involvement of the mesentery (local release of serotonin) Carcinoid metastatic disease in the small-bowel mesentery manifests - hypervascular enhancing soft-tissue mass with well-defined or spiculated borders. Dystrophic calcification is present in up to 40% of carcinoid tumours. Malignant mesothelioma Middle-aged man, Asbestos exposure. DDX carcinomatosis: sheet like, no calcification. Diffuse or nodular thickening. Omental thickening. T1 low, T2 high. Cystic mesothelioma Peritoneal cyst Women premenopausal with a history of abdominopelvic surgery. PID, endometriosis. T1 low. Fibromatosis, or desmoid tumor Mesenteric Fibromatosis. The commonest primary, proliferation of fibrous tissue. FAP, Gardner syndrome. Locally aggressive. CT homogeneous, MRI low T1, variable T2. Contrast enhancement. Complication: mesenteric ischemia. Soft-tissue mass in the mesentery (black arrows), resulting in segmental jejunal ischemia, manifested as symmetrical wall thickening. Pancreas cystic masses Mucinous cystadenoma Mother Middle-aged Malignant Few cysts, large >2cm If see solid elements, contrast enhanced nodule or mass consider mucinous cystadenocarcinoma – malignant transformation CEA “mother carries embryo” Surgical resection Mucinous Cystadenoma. Macrocystis mass in the pancreas (arrow) with thin septations. Multiple cystic liver metastases present, with one exophytic metastasis in the left lobe. Serous Cystadenoma. Grandmother Benign VHL Von Hippel-Lindau Many small cysts Central scar that enhances. Stellate calcification If small looks solid, MRI to see cysts T 2 weighted TSE image shows a microcystic mass in the pancreatic head. Only one of the innumerable cysts has a considerable size. (B) Gadolinium-enhanced T 1 weighted GRE image demonstrates enhancement of the septations and of the central scar. No other solid components are seen. Mucinous cystadenoma Serous cystadenoma IPMN – main duct type IPMN – side duct type IPMN - mixed Age Mother Middle-aged Grandmother Old Commonest Commonest Origin Epithelium of main duct, produce mucin Spectrum Malignant Benign Associations VHL Von Hippel-Lindau Number, size Few cysts, large >2cm Many small cysts Features If see solid elements, contrast enhanced nodule or mass consider mucinous cystadenocarcinoma – malignant transformation Central scar that enhances Stellate calcification If small looks solid, MRI to see cysts Diffuse or segmental duct dilation Higher risk of malignancy Diffuse or segmental duct dilation Saccular dilation Diffuse or segmental duct dilation Solid parts suspicious for malignancy FNA CEA “mother carries embryo” Management Surgical resection Surgical removal as potential for malignancy Imaging follow-up if <3cm IPMN = intraductal papillary mucinous tumor IPMN worrisome features IPMN high-risk stigmata Cyst > 3cm of pancreatic head Jaundice + cystic lesion of pancreatic head Enhancing mural nodule <5mm Enhancing mural nodule >5mm Thick, enhanced cyst wall MPD 5-9mm MPD >10mm Abrupt change in MDP caliber Upstream atrophy of pancreas Lymphadenopathy Rapid cyst growth rate >5mm/2y Endosonography RESECT CT and MRI perform similarly to differentiate benign and malignant IPMN Best way to differentiate them from pancreatic pseudocyst is FNA – pseudocyst has very high amylase. Pancreatic metastases Origin from Lung cancer – hypovascular metastases Breast cancer RCC Renal cancer Isolated metastasis or Multiple, hypervascular metastases Melanoma “Black Lives Matter + RCC” Gallbladder stones 15% of population US best for diagnosis 80% asymptomatic Increase risk of carcinoma 70% predominantly cholesterol 30% black pigmented – calcium bilirubinate Radioopaque only <10% seen on AXR On CT can see a minority Some small stones do not have acoustic shadow but DDx from polyps because they are mobile Non-visualization of GB on US due to: Non-fasting Cholecystectomy Edematous cholecystitis Gallstones with double arc shadow Gallbladder wall thickening Non fasting state Edematous state Hepatitis Pancreatitis Adenomatosis Carcinoma GB varices. Corrosive Ingestion Necrosis – slighing of mucosa and submucosa, fill thickness necrosis may lead to perforation. Granulation, fibrosis and stricture. -> obstructed stomach. a week or two, fibrotic contraction of the stomach becomes evident. In severe cases, the lumen of the stomach may be no larger than that of the duodenal bulb. Radiation-induced bowel damage Early phase is mucosal injury, colitis. Chronic changes – proctitis with possible ulceration. Rectal stricture, fistula formation with vagina or bladder. Pseudomembranous Colitis Clostridium difficil, gross wall thickening, with marked mucosal enhancement and extensive low attenuation from submucosal oedema. Causes: antibiotics, Immunocompromised patients, ischemic colitis, Sever edema from cirrhosis. Neutropenic Colitis Causes: Chemotherapy with bone marrow transplantation. Pneumatosis is common -21% Typical: right sided, caecum, mesenteric stranding, small-bowel involvement. Tuberculosis - may be secondary to pulmonary TB - drinking unpasteurized milk. Imaging: Contracted caecum with ileocecal valve. Dilated terminal ileum. Short hourglass stricture demarcated from normal bowel. Ascites, peritoneal involvement, lymphadenopathy. Lymph nodes central caseous necrosis. Hypoechoic center, peripheral enhancement. Prostatic cancer 90% prostatic adenocarcinoma Gleason score from 1-5 describes the dominant pattern and most aggressive non-dominant pattern from 2-10 Clinically significant with ISUP grade of 2 or more BPH Benign prostatic hyperplasia Arise in transitional zone On MRI: Hyperintense T2 and hypointense T2 nodules, well-circumscribed Can be hypervascular Can have foci of low ADC T1 sequence: not useful as lesions are isointense to normal prostate T1 only used for assessment of post-biopsy hemorrhage with high T1 Interval of 6 weeks between biopsy and MRI to avoid false positives due to hemorrhage that is high T1, low T2 T2 sequence: lower signal intensity correlates with higher Gleason 3 glandular zones = Peripheral zone (posterior-inferior), hyperintense T2, higher ADC values 80% most of prostate carcinoma Does not look like a nodule, intertwined with normal tissue – hard to detect Prostatitis – exclusively in peripheral zone Transitional zone (surrounds urethra) 20%–25% of PCa foci arise from the transition zone Central zone T2, P – peripheral zone. C – central and transitional zone. PI-RADS is used to assess, on a 5-point scale, the likelihood that mp-MRI findings correlate with the presence of a clinically significant PCa for each lesion in the prostate gland, ranging from a very low (PI-RADS 1) to a very high (PI-RADS 5) likelihood. T 2 weighted imaging, diffusion-weighted imaging (DWI) and dynamic contrast-enhanced MRI (DCE). In the peripheral zone, DWI is the primary determining sequence. Transition zone, T 2 weighted is dominant T1 high signal in the peripheral zone – hemorrhage. BPH “transition to cancer” – older men transitional zone. Hyperplasia of the prostatic tissue. Hodules, hypervascular, low ADC. The peripheral zone is depicted with high signal intensity on the T 2 weighted images Sagittal T 2weighted image (A) and T 1 weighted image (B) of the whole spine of a 71-year-old patient with bone-metastasised castrate-resistant prostate cancer. The images show metastatic lesions in C3, C5, C6 and L5, with low signal intensity in the metastases on both T 1 and T 2 weighted images Parasitic splenic cysts are typically caused by Echinococcus. These cysts appear at CT and US as sharply marginated, round/ovoid water-density masses and may have ring-like calcification; small daughter cysts may be present at the periphery of the main cyst. Echinococcus cysts may be heterogeneous secondary to internal debris and hydatid sand Splenic metastases are relatively uncommon, 50% - mts melanoma. 50% from breasr, lung, colon, ovary, endometrium, prostate. On CT and MR, enhancement may be present in the periphery and within viable internal septa. Aspiration or biopsy may be required to confirm the diagnosis. Sarcoidosis Splenomegaly. Nodular lesions 2-3 cm. Or necrotic mass with focal calcification. Haemosiderosis CT – high. MRI – T2 i-T1 low due to iron. CHEST Causes of Bilateral Upper Lobe Fibrosis Tuberculosis (including atypical mycobacterial infections) Sarcoidosis Histoplasmosis Allergic bronchopulmonary aspergillosis Chronic extrinsic allergic alveolitis Ankylosing spondylitis Progressive massive fibrosis (distinctive mass-like opacities) Idiopathic pleuroparenchymal fibroelastosis Sarcoidosis Solid micronodules clustered into a major opacity with a periphery of smaller nodules (‘galaxy sign’, Severe traction bronchiectasis selectively located in the upper lobe, along with signs of local volume loss. Lymph nodes may calcify -eggshell also seen in silicosis and histoplasmosis. The calcification is of variable intensity and may even be relatively light with homogeneous representation over the whole lymph node, into the so-called ‘icing sugar’ pattern. About 40% of patients presenting with nodal enlargement will develop parenchymal opacities, usually within a year, and of these about one-third will go on to have persistent (fibrotic) changes. Usually, nodal enlargement does not develop after parenchymal opacities have appeared. Well-defined, smooth or irregular nodules, measuring 2–4 mm, in a perilymphatic distribution (i.e. mainly along interlobar fissures, peribronchovascular interstitium and interlobular septa), most extensive in the upper lobes10—20% - Patchy airspace consolidation. Fibrous shadowing – coarse linear opacity, upper/middle lobe predominance. Volume loss of upper hilum. Enhancing Lymph Nodes: Castleman. Hyper vascular mts Melanoma RCC Carcinoid Papillary thyroid cancer. Kaposi sarcoma. Castleman : Lymph node hyperplasia uncertain aetiology. Lymph node enlargement in many sites in the body. The lymph node mass is often localised to one area, can be huge and may be very vascular. The nodes may calcify and may show striking contrast media enhancement.   BRONCHOGENIC CYST Usually asymptomatic Symptomatic if super-infected, has rapid growth due to internal haemorrhage, or compresses the airway Most frequently located adjacent to the central airways in the subcarina Solitary spherical or oval mass containing simple, low-attenuation fluid Thin-walled unless super-infected Can contain proteinaceous fluid, blood, or rarely, milk of calcium CT and MRI demonstrate no internal enhancement Imaging features similar to an oesophageal duplication cyst Contrast media-enhanced magnetic resonance imaging reveals intense enhancement of the wall of the infected bronchogenic cyst Oesophageal Duplication Cysts Childhood Asymptomatic May become infected or ectopic gastric mucosa within the cyst may cause hemorrhage or perforation. Wall may be thicker, the cyst may assume a more tubular shape and it may be in more intimate contact with the esophagus. Constrictive pericarditis and restrictive cardiomyopathy Causes: The most common causes of constrictive cardiac surgery radiation therapy. Other causes include infection (viral, tuberculous), connective tissue disease, uraemia, neoplasm or idiopathic Idiopathic. Secondary findings of diastolic heart failure due to the severe constrictive pericarditis are seen, manifesting as bilateral pleural effusions, ascites, inferior vena cava and hepatic venous distension, and a ‘nutmeg’ liver parenchyma due to liver congestion and development of hepatic cirrhosis Hallmarks: Restriction in diastolic filling. Pericardial thickening, calcification and abnormal diastolic ventricular function.   Lymphangioleiomyomatosis Alone or with TS tuberous sclerosis complex Renal angiomyolipoma “LAM associated with AML” On imaging: Normal or increased lung volume Causes pneumothorax Pleural effusions with chyle Characteristic diffuse thin-walled cysts with no zonal predilection, round shape, normal lung parenchyma DDx Lung LCH Langerhans Cell Histiocytosis Progression from ill-defined nodules (which cavitate) to a combination of cysts and nodules. Upper zones predominant abnormalities with substantial sparing of lower lung, typically seen in adult. male-to-female ratio is about 4 : 1. Bilateral, symmetrical findings Upper zone, pathognomonic sparing of lower zones and costophrenic angles Exception in children Reticulonodular shadowing Nodules vary in size but mostly small, solid and subsolid Cavity Cysts in late disease, with bizarre shape, that cause spontaneous pneumothorax Intrathoracic Manifestations of Rheumatoid Disease Pleural effusion or thickening Interstitial fibrosis (most frequently usual interstitial pneumonia type) Constrictive obliterative bronchiolitis Bronchiectasis Organising pneumonia Follicular bronchiolitis Drug-induced lung disease (methotrexate) Necrobiotic nodules/Caplan syndrome Rheumatoid Arthritis With a Usual Interstitial Pneumonia-Type Pattern. CT: peripheral reticular abnormality and honeycombing are indistinguishable from that of usual interstitial pneumonia. Thymic cysts Can be simple, part of a thymoma or follow radiation to the thymus for Hodgkin’s disease On MRI, thymic cysts demonstrate typical characteristics of fluid with low T 1 and high T 2 signal intensity. Thymoma / Cystic thymoma Most common thymus tumor in adults and anterior mediastinum Earlier age of diagnosis if associated with myasthenia gravis MG 50% with thymoma have MG 20% with MG have thymoma Difficult to DDx thymoma from thymus hyperplasia in MG Associated with: MG Hypogammaglobulinemia Red cell aplasia Spherical or oval with lobulated borders Can have cystic changes, hemorrhage, necrosis Can have punctate or curvilinear calcification On CT: Homogeneous density, uniform enhancement On MRI: normal thymus has intermediate T1 and T2, lower than fat and higher than muscle In thymoma low T1, high T2 Metastases to: Pleura via direct spread MRI better than CT to show mediastinal involvement Features of malignant thymoma/invasive thymoma: 5% at diagnosis 1-Absence of capsule 2-Extension into capsule 3-Pleural thickening, nodularity, pleural effusion 4-Associated with pleural implants DDx thymic carcinoma Fat planes obliteration but absence of obliteration does not exclude capsular invasion Treat by surgical resection (90%) arise in the superior aspect of the anterior mediastinum projecting from the left or right heart border, or lying close to the cardiophrenic angles. Cystic Thymoma. a mixed cystic and solid mass located in the anterior mediastinum, adjacent to the right atrium and right ventricle. (C) Steady-state free precession sequence shows a large mural nodule within a larger cystic component of the mass. T 1 with fat saturation show no fat within this lesion. (F) T 1 weighted, fat-saturated image obtained after contrast heterogeneous enhancement of the solid component. F T1+ Teratomas are the most common mediastinal germ-cell tumour and most are cystic. Teratomas are found at all ages, particularly in adolescents and young adults. Cystic Teratoma. An 8-year-old girl with intermittent chest pain for 2 years was found to have an anterior mediastinal mass on a chest radiograph (A). Contrast media-enhanced computed tomography images in (B) coronal and (C) sagittal projections show a mostly cystic lesion in the anterior mediastinum, with a thick, nodular, and enhancing wall. Pathological examination after surgical excision of the mass showed typical features of a mature teratoma MRI: Low T 1 intensity and high T 2 intensity, and fat appears as high T 1 intensity with signal loss on fat-saturation sequence. Fat is virtually diagnostic of teratoma.. Round Atelectasis. High-resolution computed tomography in axial (A) and sagittal reformation (B) show the subpleural consolidation and the curve bronchovascular bundle (‘comet tail’) towards the atelectasis. Associated with pleural thickening Posterior lower lobes Next to visceral pleura due to pleural infolding from: exposure to mineral dust: asbestosis, pneumoconiosis  exudative pleuritis: tuberculosis, hemothorax   less commonly seen in histoplasmosis, legionella, end-stage renal disease, sarcoidosis Comet tail sign of crowded bronchovascular bundle from the border of the mass to the hilum Strong, homogeneous enhancement indicative of atelectasis DDx lung cancer Volume loss of affected lobe is a key sign HIGH-GRADE INTRAMEDULLARY (CONVENTIONAL) OSTEOSARCOMA distal femur is the most common site. the proximal tibia. the proximal humerus. A, Oblique radiograph shows an aggressive, predominately lytic lesion in the proximal tibia metaphysis. Note cortical breakthrough (arrow) and wide zone of transition. A very small region of sclerosis within the bone (arrowheads) could represent either tumor matrix or reactive bone formation. B, Coronal proton-density–weighted MR imaging shows that the lesion is larger than suggested by radiography and confirms Cortical breakthrough medially. Conventional osteosarcoma x-ray: distal femoral metaphysis aggressive-appearing immature tumor osteoid in both the bone and soft-tissue mass. aggressive periosteal reaction and a wide zone of transition. GIANT CELL TUMOR OF BONE Giant cell tumor (GCT) is a common, usually benign neoplasm 5% of primary bone tumors and 20% of all benign primary bone tumors. It consists of connective tissue, multinucleated osteoclastic giant cells, and a fibrous stroma Typical lesion lytic geographic at the end of a long bone, without margin sclerosis. In the skeletally mature the lesion extends to the subchondral bone. Most common sites: About the knee, distal radius or ulna Spine: Sacrum or body of vertebra Originates in the metaphysis Rare before physeal fusion, most commonly between 20 and 40 years of age Most are benign, but may metastasize to lung Approximately 25% to 50% local recurrence rate; higher with less aggressive surgery. Recurrent tumors may behave more aggressively. Lytic lesion in the distal femoral metaphysis (arrows), extending to the subchondral bone at the anterior portion of the femoral condyle and the roof of the intercondylar notch. There is no matrix, and the zone of transition is narrow and lacks a sclerotic margins. Eccentrically located lytic distal femoral metaphysis and extending to the subchondral bone plate. The zone of transition is narrow, but the margin is not particularly sclerotic. There is no host reaction. Appearance is typical of GCT. B, Axial T2-weighted fat-saturated MR image of the same lesion shows a heterogeneously hyperintense lesion with mild osseous expansion. There are nodular regions of low signal within about one fourth of the lesion, a finding characteristic of GCT. The common femoral artery (CFA) is the most frequent access site for angiography. The majority of CFA punctures are retrograde (against arterial blood flow) as opposed to antegrade (in the direction of arterial blood flow). In a single-wall puncture, the needle is advanced a few millimeters after the tip touches the artery, just through the anterior wall of the vessel. decreasing the chance of a bleeding complication. If the needle tip only partially enters the lumen, there will be good blood return but the guidewire can pass into the subintimal layer as it exits the needle (Fig. 2-32). he common femoral artery (CFA) (arrow) and common femoral vein (CFV) (arrowhead) within the femoral sheath. EUS is superior to CT and PET-CT for T staging. The sensitivity and specificity for identifying the various T stages of oesophageal cancer is high. If the tumour is not traversable with the standard echoendoscope, the T stage is almost always T3 or T4. The number of abnormal lymph nodes seen on EUS correlates closely with patient survival. For nodal disease, EUS has a sensitivity higher than that of PET-CT or CT, but it is less specific. Intussusception: Most common surgical emergency Peak 5-9 month. Ileocolic most common. Most 90% have no lead point – due to lymphadenopathy. In young infants or older than 6 years, more likely to be caused by secondary lead point due to NJ tube Polyps Meckel diverticulum Duplication cyst Lymphoma Linear trancducer. Free intraperitoneal fluid – commonly seen. Stable patient - Always attempt hydrostatic reduction / pneumostatic reduction, with exceptions Free air – rare, dont need xray. Peritonitis Reduction of ileocolic has a success rate of 80%. Doughnut’ or ‘target sign’ (arrowheads) caused by the multiple layers of bowel and the pathognomonic hyperechoic semilunar appearance of the mesenteric fat within the intussusceptum (asterisk). (B) The longitudinal view reveals the typical ‘sandwich’ appearance caused by the multiple layers of bowel wall and mesenteric fat (asterisk). Henoch–Schönlein Purpura acute small vessel vasculitis. purpuric skin lesions (without thrombocytopenia) GI manifestations, arthritis or nephritis. Abdominal pain is a common symptom, the GI involvement is caused by oedema, bleeding, ulceration and intussusception of the intestine. US sensitivity of up to 100%. Intussusceptionin HSP is usually ileo-ileal. Ultrasound is the imaging investigation of choice in HSP: uni- or multifocal thickening of the bowel wall accompanied by reduced peristalsis, with normal or slightly dilated bowel loops between the thickened segments intraperitoneal free fluid. IBD children Small children colon often affected. Fistula formation Small bowel wall thickness id 1.5-3 mm. Colon 2-3 mm. Small bowel intussusception – If thick wall – edema -> surgery Mesenteric cyst – Intraabdominal lymphangioma Cystic lesion with thick wall, different from enteric duplication cyst (double layering). Ddx ascites in cade of large mesenteric lymphangioma. Mesenteric border of the small bowel. Pyloric stenosis Length of pyloric canal 17 mm. Transverse diameter of the pyloric muscle above 3 mm. Meckel – Antimesenteric border of the ilium. 60 cm from the iliocacal junction. Contain gastric/pancreatic mucosa. If entrapped to the hernia – Littre hernia. Diagnosis – interoperable. If hemorrhagic – 95% gastric mucosal – Tc pertechnetate scintigraphy. Saccular, blind-ending pouch on the antimesenteric border of the ileum with a triradiate fold pattern converging with the ileum. Hepatoblastoma Uncommon in the first few months of life and after 3 years of age. Associations: Beckwith–Wiedemann syndrome biliary atresia. Thrombocytosis raised serum α-fetoprotein (AFP) for age (raised AFP is also associated with the rarer yolk sac tumor). Staging is based on the number of adjoining liver sections free from tumor, venous encasement/invasion, rupture and metastases. Metastases are most commonly in the lungs, so chest CT is part of the staging procedure. This tumour occurs at any age but most commonly in children less than 3 years old. It is the third commonest abdominal childhood tumour, after neuroblastoma and Wilms’ tumour, and is associated with markedly elevated serum AFP levels. Histologically, it is composed of primitive hepatocytes, often with mesenchymal components. On imaging, the tumor presents as a large heterogeneous mass but may also appear composed of multiple confluent nodules. There may be central areas of necrosis, and enhancement may be seen in the arterial phase on CT. Punctate calcification is a common finding on US and CT. Liver metastases in children most frequently from neuroblastoma lymphoproliferative disease, nephroblastoma sarcomas. Differentials for multifocal liver lesions include multifocal vascular neoplasm, infection, regenerating nodules, focal nodular hyperplasia, angiomyolipoma, fibropolycystic disease and peliosis hepatis. Neuroblastoma 85% calcifications – peripheral, coarse, amorphous DDx Wilms’ tumor only in 10% Both displaces and encases vessels Can be detected antenatally 50% have metastatic disease at diagnosis – very bad prognosis DDx Wilms tumor with excellent prognosis Sites of metastases: Bone marrow Bones Lymph nodes Lung – rare Brain – rare Orbital – proptosis Cervical and thoracic involvement of stellate ganglion – Horner syndrome Liver metastases: either as diffuse infiltration or hypoenhancing mass “closer to liver” DDx with hepatoblastoma – both have calcifications but hepatoblastoma has heterogeneous enhancement In infants younger than 1 massive hepatic metastases, palpable nodes, bone marrow lesions Paradoxically better prognosis and recovery. Risk of severe respiratory complications due to massive hepatomegaly Paraneoplastic syndromes: HTN due to hormone production Watery diarrhea due to VIP Myoclonic encephalopathy of infancy MEI 90% most have high levels of catecholamines (noradrenaline, dopamine) in urine Initial diagnosis of abdominal NB is via US or CXR Use PET CT to detect metastases – 123I-mIBG scintigraphy and 99mTc-MDP bone scintigraphy Radiographs Calcified mass in thorax or abdomen US Adrenal glands can appear cystic in most cases – non specific DDx especially adrenal hemorrhage Palpable or large >5cm mass probably neuroblastoma Remains stable or grows at follow-up Retroperitoneal location Variable echogenicity hyperechoic foci being calcifications hypoechoic areas being hemorrhage or necrosis Highly vascular on Doppler CT Calcifications in 85% of cases MRI Performed for any paraspinal mass suspected to extend into extradural space Radionuclide radiology 123I-mIBG scintigraphy to diagnose the mass / characterize it, localizing the primary tumor in MEI and evaluating metastases and follow-up Performed in all patients as 2/3 have bony metastases at diagnosis Image Defined Risk Factors Based on CT and MRI Determine whether tumor is resectable or not resectable Contact: it is an IDRF only for renal vessels Encasement: for vessels >50% of its circumference Compression: of airway Separation: layer between tumors and other structures Infiltration: of tumor in structures other than vessels Cryptorchidism Isolated or associated with: Prune Belly syndrome Beckwith-Wiedemann syndrome Rubella DDx: Mumps causes orchitis “Mumps orchitis” Renal agenesis Prevalence parallels gestational age: 100% of premature infants <900g are affected 4% in infants weighing >2500g 1% at 1 year as most resolve spontaneously Can be bilateral in minority 10-25% (Soroka) Monitor until 1 year of age Can be anywhere in canal – from retroperitoneum to inguinal canal 80% most are in inguinal region and usually palpable Increase risk of: Infertility – surgery decreases infertility Seminoma / testicular malignancy – higher risk of malignancy remains after orchidoplexy On US: look in transverse plane, can be atrophic 97% highly sensitive for palpable testes US less reliable for non-palpable testes with 75% US poor for intra-abdominal testes – 45-75% sensitive On MRI: low T1 high T2 Improved detection sensitivity and specificity with DWI use Patterns of Brain Injury in the Preterm Neonate US screening is advocated in all babies born at less than 30 to 32 weeks’ gestational age US examinations beginning as early as possible and then as often as daily in the first 4 to 7 days, then weekly with a final study before discharge. At minimum, all preterm babies admitted to neonatal units should undergo initial US with further imaging at 10 days and finally just before discharge. Therefore MR should be reserved for the investigation of babies with neurological symptoms or signs. On US: Hyperechoic white matter – flares After a few weeks development of cysts On MRI: Restricted diffusion Cysts in periventricular and deep white matter that have central free diffusion Cysts are resorbed over time Ventricular enlargement – ventriculomegaly Thinning of periventricular white matter Irregular outline of body of lateral ventricles Day 10 of life: sagittal image increased heterogeneous echogenicity of the periventricular white matter (arrow). Day 25 of life: sagittal images demonstrating multiple cysts of the periventricular white matter (arrows T2 weighted axial images (C and D) demonstrating thinning of the periventricular white matter, irregular outline of the lateral ventricles (arrows) and periventricular cysts (arrowheads). Brain haemorrhagic disease germinal matrix haemorrhage (GMH) intraventricular haemorrhage (IVH) paraventricular haemorrhagic infarct (PHI). GMH may appear 24h after birth and starts from the germinal matrix located under the ventricular ependyma. Regression of the germinal matrix starts at 12 to 16 gestational weeks and disappears at term. At approximately 24 weeks, germinal matrix is present under the frontal horns of the lateral ventricles. Brain US shows an ovoid lesion located anterior to the caudothalamic groove, initially homogeneously hyperechogenic, then heterogeneously hyperechogenic and finally cystic. IVH may result from rupture of GMH into the ventricles or from bleeding at the level of the choroid plexuses. MRI demonstrates a variety of signal intensities, depending on the age of haemorrhage, with high signal at the subacute stage and signal void at the chronic stage. Posthemorrhagic hydrocephalus may appear as complication of large IVH. PHI associated with IVH compression and obstruction of terminal veins lying under the germinal matrix. Brain US typically shows a frontoparietal hyperechogenic triangular lesion pointing towards the lateral ventricle. Liquefaction and sometimes communication of the lesion with the lateral ventricle are observed at the latter stages leading to a porencephalic cyst. Lesions lying anterior to the motor tracts carry a better neurological outcome. Early MRI demonstrates a haemorrhagic paraventricular lesion associated with IVH; late MRI shows a cystic lesion surrounded by gliosis and communicating with the lateral ventricle. Centrally cystic ovoid lesion located at the right lateral ventricle, anterior to the caudothalamic groove. Brain US shows echogenic material within the lateral ventricles, sometimes extending into the third ventricle echogenic material into the right lateral ventricle -blood. Midline sagittal (C) echogenic clot pending from the foramen of Monro into the third ventricle (arrow). -echogenic venous infarct adjacent to right lateral ventricle (arrow). liquefaction of the lesion and the formation of a cavity communicating with the lateral ventricle. NORMAL MYELINATION Oligodendrocytes produce it Posterior-to-anterior and caudal-to-cranial and central to peripheral pattern until 2 years None initially and so underdeveloped white matter is low T1, high T2 Process includes increase in myelin, decrease in water in white matter With time there is T1 and T2 shortening of white matter due to myelin = high T1, low T2 T1 complete at 10 months After 6 months T1 less sensitive (first 6 months: T1 more sensitive) T2 at 2 years first 6 months T2 less sensitive (after 6 months: T2 more sensitive) Persistent high T2 signal in “terminal myelination zones” in peritrigonal areas into adulthood / around trigone T1 shortening the posterior limb of the internal capsule. This progresses posteriorly to anteriorly and centrally to peripherally until by 12 months the brain appears fully myelinated. At 3 months Internal capsules Splenium of corpus callosum At 6 months Entire corpus callosum At 8 months Internal capsule T1 shortening = high signal T2 shortening = low signal Full term dorsal medulla brainstem cerebellar peduncles 1/3 of posterior limb of internal capsule Central corona radiata At 3 months Internal capsules Splenium of corpus callosum At 6 months Entire corpus callosum At 8 months Internal capsule Normal Gyral Development 16 w - interhemispheric fissure and Sylvian fissures. 22 w - Other primary sulci, such as the callosal sulcus and parieto-occipital fissure. 27 w - central sulcus Causes of neonatal abdominal mass lesions Complicated meconium ileus Dilated bowel proximal to an obstruction Mesenteric or duplication cyst Abscess Genitourinary causes: Hydronephrosis - commonest Renal cystic disease Mesoblastic nephroma Wilms’ tumour Adrenal haemorrhage Neuroblastoma Retroperitoneal teratoma Ovarian cyst Hydrometrocolpos Hemangioendothelioma Hepatoblastoma Choledochal, hepatic or splenic cysts Causes of pediatric abdominal calcifications Complicated meconium ileus Intraluminal calcifications: Low obstruction Anorectal malformations with a fistula to the urinary tract Adrenal: Haemorrhage Neuroblastoma Hepatobiliary: Haemangioendothelioma Hepatoblastoma TORCH infections Duplication cysts and mesenteric cysts Nephrocalcinosis Intravascular thrombus Acute aortic syndrome:  Aortic dissection: intimal disruption that allows blood to track through a dissection plane in the media.  Intramural hematoma: intramural hemorrhage from vasa vasorum or bleeding at the base of a penetrating ulcer (can appear similar to thrombosis of a dissection false lumen).  Penetrating aortic ulcer: ulcerating atherosclerotic lesion that penetrates into the media. MSK Gout Sodium urate crystal–induced arthropathy Middle-aged to older adult men Chronic disease processes may predispose to gout Normal bone density Cartilage often intact even late in the disease Erosions: Sharply marginated and may be intraarticular or paraarticular (“nonmarginal”) Overhanging edge of a paraarticular erosion is virtually Pathognomonic: First metatarsophalangeal, distal interphalangeal, and proximal interphalangeal joints PIP and patella most frequent joints Gouty tophus radiographs: May show amorphous calcification (calcium urate) Gouty tophus magnetic resonance imaging: Low signal intensity on T1-weighted, variably high or low signal on T2-weighted, enhances with gadolinium Laboratory abnormalities include hyperuricemia and sodium urate crystals in synovial fluid. The crystals are needle- or rod-shaped and negatively birefringent when viewed with polarized light microscopy. First metatarsophalangeal PIP -2, DIP – 5th Juxtraarticular erosions, calcified tophy Faintly calcified soft-tissue mass adjacent to the ulnar styloid (arrows). Bones appear normal Gout simulating rheumatoid arthritis (RA). However, the normal bone density and the distinctness of the erosions should suggest gout as a diagnosis, even in the absence of tophus formation. Also note the carpal erosions, including a large erosion in the capitate (black arrow) 50-year-old man shows erosions in a proximal distribution (arrowheads) suggestive of RA. Gout, MR imaging. MR images in a patient with tophaceous gout of the fifth metacarpophalangeal joint show the mass to have intermediate to low signal intensity in A and B (arrows), and intense enhancement in C (arrows), which are typical MR findings in gout. Fifth finger coronal T1-weighted (A), inversion recovery (B), and fat-suppressed contrast-enhanced T1-weighted (C) Ovarian Fibroma. (B) T1, and (C) T2 weighted axial images showing the typical findings of a fibroma on magnetic resonance imaging, with low signal on T1 and T2 weighted images (asterisk). U, Uterus. MRI, where they demonstrate characteristic iso- to hypointense T2 and T1 signal Dermoid (A) Axial portal venous contrast-enhanced computed tomography (CT) of a large dermoid cyst demonstrating calcification (asterisk) and a fat-fluid level (black arrows) (C) Sagittal portal venous contrast-enhanced CT demonstrating an enhancing mass extending through the wall of a large ovarian dermoid (white arrows). On histology the lesion was confirmed to be a squamous cell carcinoma arising from the ovarian dermoid. B, Bladder; U, uterus. Dermoid cyst T1 weighted and (B) T1 weighted fat-saturation There is a left adnexal mass (asterisk) with areas of high and intermediate signal on the T1 weighted image, and suppression of the high signal from fat on the T1 weighted fat-saturation sequence. Mature cystic teratomas, or ovarian dermoid, are derived from one or more of the three germ cell layers. B Complications: torsion (16%), rupture (1%–4%), infection (1%), malignant degeneration (1%–2%) auto-immune syndromes (<1%) such as autoimmune haemolytic anaemia and anti-N-methyl-D-aspartate receptor encephalitis. Mucinous cystadenomas 15%–25% of all ovarian tumours. Contain: mucinous material, multiloculated with thin septa and can grow to a large size. The locules can demonstrate variable signal on MRI, depending on the combination of proteinaceous, mucinous and hemorrhagic content. Axial T2 weighted MRI demonstrating a left serous (white arrow) and right multiloculated mucinous cystadenoma (black arrow). Mucinous Cystadenoma. Sagittal T2 weighted magnetic resonance imaging (MRI) and (B) axial T1 weighted fat-suppressed MRI demonstrating multiple different signal intensity locules within a mucous cystadenoma in keeping with mucin with differing protein content (black arrow). Diagram of Enhancement Patterns of Adnexal Lesions. Postoperative Spine  Plain radiographs are used to assess obvious hardware migration, loosening or breakage. Flexion and extension views allow dynamic evaluation for instability  CT allows precise evaluation of implant position, alignment and integrity  MRI is the technique of choice to assess soft tissues and neural structure MRI :identifying the extent of haemorrhage and compression of neural structures. Findings include an epidural mass with a T1 signal dependent on the age of the haematoma (iso- or hypointense in acute haemorrhage, hyperintense in chronic haematoma) and heterogeneously hyperintense on T2 weighted sequences, with no contrast enhancement Epidural Haematoma. epidural mass slightly hyperintense to spinal cord on T1 weighted images (A) Heterogeneous signal on T2 sequence No enhancement following gadolinium administration. Extravasation of CSF into surrounding tissues leads to formation of a pseudomeningocele. may be associated with signs of intracranial hypotension (CSF leakage syndrome) dural thickening and enhancement, ‘sagging’ midbrain, tonsillar herniation, venous distension, pituitary gland enlargement and subdural haematomas or hygromas. T1 and T2 fluid density collection Early complications: Hemorrhage CSF leak Infection Pseudomeningocele Late complications: Hardware failure Displacement Pseudoarthrosis and instability Adjacent segment disease Failed back surgery syndrome – persistent or recurrent pain after spinal surgery Use MRI with contrast enhancement Failed back surgery syndrome (FBSS Between 10-40% Residual or recurrent disc herniations are common following spinal surgery and can present with persistent or recurrent pain Recurrence of symptoms after a 6-month pain-free period postoperatively Seen in 7% to 12% of FBSS cases In the first few days after surgery it is difficult to differentiate the residual disc herniation from inflammatory tissue and debris In the following weeks the inflammatory process and mass effect subside and avidly enhancing granulation tissue forms After several months the granulation tissue reorganizes to form epidural fibrosis, which demonstrates diffuse but weak enhancement Differentiation between epidural scar and disc material is one of the most important and challenging aspects of postoperative spine imaging Both disc material and epidural fibrosis are low T1 and high T2 Gadolinium-enhanced T1 weighted images are crucial in their differentiation - accuracy of 96% to 100% Recurrent or residual herniated disc material does not enhance, or there is mild enhancement at the periphery It is important to remember that contrast medium will penetrate the disc with time and the central part may show enhancement if imaging is delayed It is therefore crucial that post-gadolinium images are obtained immediately after contrast injection A herniated disc usually has smooth margins, lies anterolateral in the epidural space and tends to displace or compress the nerve roots and theca On the other hand, epidural fibrotic tissue enhances early and uniformly, has irregular configuration with minimal mass effect and can occupy anterior-to-posterior aspects of the epidural space. It can also encase and retract the theca and nerve roots rather than displace them Example of a Recurrent Disc Herniation. Unenhanced T1 epidural lesion abutting the left anterior aspect of the thecal sac T1 + peripheral enhancement, but the centre of the lesion remains of low signal. Epidural Fibrosis. (A) T1 - epidural lesion adjacent to the left anterior aspect of the theca. (B) T1 + avid enhancement of the scar. Exiting nerve root (arrow) is surrounded by the enhancing tissue. Exam 2016 Neuro STROKE When vessels are fully dilated and reaches limit, CBF starts to decline Loss of normal neuronal electrical function when CBF<20 May be reversible Irreversible when CBF<10 Moderate ischemia with CBF 10-20 reversible for a few hours – penumbra Normal flow 50. Gold-standard treatment is still TPA LVO large vessel occlusion gold-standard treatment is TPA + mechanical thrombectomy Benefits seen up to 24h after recanalization Large vessel occlusion stroke / large vessel thromboembolic stroke 40% From most common: Carotid bifurcation Intracranial ICA Proximal MCA Vertebral artery origins Distal VA Basilar artery Cardioembolic stroke 15-30% Intracardiac thrombus due to: MI, aneurysm, enlarged left atrial appendage, paroxysmal AF, valvular disease, right-to-left shunt, cardiac tumors. ASPECTS score Two slices at Basal ganglia and internal capsule Upper margin of bodies of lateral ventricles 10 regions Normal brain has score of 10 1 point deducted for each involved area Score <7 is infarct involving >1/3 of MCA Fig. 56.7\ Alberta Stroke Program Early Computed Tomography Score (ASPECTS) for Acute Ischaemic Change on Computed Tomography. (A) Slice at the level of the basal ganglia. C, Caudate nucleus; L, lentiform nucleus; IC, internal capsule; M1, M2 and M3, middle cerebral artery (MCA) territory at the level of the ganglionic nuclei. (B) M4, M5 and M6, MCA territory at the level above the ganglionic nuclei: 1 point is deducted for each area involved. A normal computed tomography scan will have an ASPECT of 10. Stroke has both cytotoxic edema and vasogenic edema. CTA/perfusion is useful for the supratentorial circulation only and is not reliable in posterior fossa or deep nuclei infarction. Young Patient With Vasculitis Presenting With.Fluid-attenuated inversion recovery (FLAIR) demonstrates multiple foci of high signal consistent with multiple ischemic lesions. MRI offers clear superiority for diagnosis of brain infarction, can differentiate acute from old infarcts and has equal sensitivity for infarcts regardless of location. Subclavian Steal Syndrome Contrast-enhanced computed tomography demonstrates occlusion of the left subclavian artery. R reduced blood flow to the posterior fossa as a result of reversed blood flow within one vertebral artery as a result of a tight stenosis or occlusion within its parent subclavian artery Small vessel stroke / lacunar stroke 15-30% Deep perforators usually Lenticulostriate perforator arteries from M1 – lentiform, internal capsule, corona radiata infarct Thalamic branches choroidal perforators from PCA, PCom – thalamus, posterior internal capsule Basilar artery perforators – brainstem infarcts Small vessel pathology due to HTN, diabetes – ischemic microangiopathy Vasculitis, drugs, radiation Intravascular lymphoma CADASIL – cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy Borderzone infaction / Watershed ischemia Especially between MCA and ACA leptomeningeal collaterals – linear distribution of ischemia especially if deep to the superior frontal sulcus Due to local hypoperfusion or global hypoperfusion or embolic infarcts Global hypoxic-ischemic injury Due to severe hypotension or impaired blood oxygenation Impaired oxygenation such as due to carbon monoxide poisoning in anoxia – globus pallidus infarct On imaging: Can result in watershed infarcts Profound ischemia / deep ischemia causes symmetric ischemia/symmetrical hypodensity of grey matter of basal ganglia, thalami, hippocampus, cerebral cortex. pseudo subarachnoid hemorrhage – due to cerebral edema with dilated superficial venous structures due to raised ICP When profound there is reversal of the grey-white matter pattern Signal change and restricted diffusion on MRI DWI in the affected areas The hippocampal formations are also sensitive to global insults – restricted diffusion Goals in acute stroke Give TPA improves outcomes provided it is given Within 4.5hours In patients with infarct of <1/3 of MCA territory – >1/3 is contraindication for IV TPA thrombolysis <80 years old Guidelines in the UK: TPA within 4.5h and puncture within 6h Mechanical thrombectomy in patients with moderate or severe acute stroke syndrome NIHSS >5 Occlusion of intracranial ICA Occlusion of proximal MCA Pre-stroke disability score mRS <3 Use of NCCT in acute stroke Exclude hemorrhage Exclude alternative cause 30% non-vascular cause Assess infarct volume – ASPECTS – Alberta Stroke Program Early CT Score Hyperdense vessel Clinical corraboration Early imaging signs of stroke on CT Hyperdense artery Earliest sign – can be seen at onset of ictus. Thrombus may disperse so not visible Better prognosis if Sylvian fissure dot sign – M2 branch Mimic DDx MCA calcification – often bilateral Top of basilar syndrome – also hyperdense Early parenchymal signs Reduced grey matter density In early MCA stroke – reduced clarity of margins of lentiform nucleus and insular cortex Loss of insular ribbon sign / loss of conscpicuity of cortex Brain swelling – effacement of sulci. On MRI SWI: linear low signal – blooming in areas of MCA thrombus – deoxyhemoglobin in acute thrombus causing exaggerated sensitivity to susceptibility artefact afforded by SWI CT has low sensitivity for acute stroke 30% in 3 hours 60% in 24 hours Stroke window – 35:35 (@Chapter 53 says 40:40) – hypodense areas correlate with infarct core and low CBV maps. Embolic Occlusion of the Basilar Artery in a Patient Presenting With Acute-Onset Vomiting and Quadriplegia. Fluid-attenuated inversion recovery (FLAIR) image at the level of the middle cerebellar peduncles demonstrates extensive infarction in the left superior cerebellar distribution (arrows) and multiple additional punctate foci of cerebellar infarction. Pilocytic astrocytoma Cerebellar low-grade astrocytoma (WHO grade I) In up to 40% In most case the astrocytoma is a pilocytic astrocytoma (WHO grade I) Well circumcised Slow growing Associated with NF1 -15% On imaging: Vermis mass or of cerebellar hemisphere Cystic with enhancing mural nodule Solid part is hypodense on CT Cystic part is low T1, high T2 - cystic Enhances avidly and homogeneously Leptomeningeal enhancement indicates dissemination but does not indicate higher grade Common pediatric intra-axial cerebellar tumors in children Medulloblastoma Pilocytic astrocytoma Ependymoma Glioma Atypical teratoid / rhabdoid tumor Brain medulloblastoma Malignant, small, round More common than pilocytic astrocytoma More in boys 40% of posterior fossa Associated with Li-Fraumeni Peak at 7 but wide age range ( neonatal to young adult). Second peak in adults with desmoplastic type – better prognosis and seen in cerebellar hemispheres 1/3 presents with leptomeningeal metastases intracranial or intraspinal subarachnoid spread Nodular irregular leptomeningeal enhancement Pial enhancement Drop metastases in spinal cord – leptomeningeal spread On CT: Hyperdense midline vermis mass “Medulloblastoma is midline and dense due to a blast” Patchy enhancement Brainstem displaced anteriorly. Calcification, hemorrhage, necrosis On MRI: Low T2 signal compared to grey matter Characteristic on imaging: best to identify it CT hyperdense MRI low T2 Restricted diffusion on DWI Seen due to increased nucleus to cytoplasmic ratio and densely packed cells On MRS MR spectroscopy (typical of many brain tumors): Low creatine Low NAA High choline Imagine is more sensitive than cytology T1 t2 diffusion coefficient map show restricted diffusion consistent with hypercellularity. Medulloblastoma. (A) Computed tomography (CT) and (B to D) axial T 2 , apparent diffusion coefficient and diffusion magnetic resonance imaging show a mixed solid and cystic mass within the right cerebellopontine angle encroaching on the pons and fourth ventricle and causing hydrocephalus. The solid component is hyperdense on CT, is hypointense on the T 2 weighted sequence and demonstrates restricted diffusion in keeping with a cellular tumour. Despite some less typical features, such as lateral site (more usually seen in older patients and associated with the desmoplastic variant) and cystic components, on the basis of the signal characteristics this was correctly diagnosed as a medulloblastoma. Differential Diagnosis of Posterior Fossa Tumour With Computed Tomography Hyperdensity and T 2 Hypointensity Infratentorial primitive neuroectodermal embryonal tumour (medulloblastoma) or atypical teratoid/rhabdoid tumour Choroid plexus carcinoma Ewing sarcoma Chondrosarcoma Chordoma Lymphoma Langerhans cell histiocytosis Cerebellar Hemispheric Tumour in a Child With a History of Ataxia, Nausea and Vomiting Over Several Months. (A, B, D and E) Axial T 2 , coronal fluid-attenuated inversion recovery (FLAIR), coronal and sagittal T 1 enhanced magnetic resonance imaging show a left cerebellar hemispheric tumour with a large cystic component and solid homogeneously enhancing component which is bright on T 2 weighted sequences (compare with the images of posterior fossa medulloblastoma, Figs 76.57 and 76.58 ). The solid component is not restricted on the diffusion- weighted image (C) and apparent diffusion coefficient map (F) compared with medulloblastoma and there is free diffusion in the cystic component. Pilocytic astrocytoma may present with diffuse nodular enhancement of the leptomeninges, indicating intracranial or intraspinal pial dissemination. This is typically seen with WHO grade I tumours, does not imply a higher-grade tumour and, like the tumour primary, tends to grow slowly. Ependymomas (WHO grade II) account for approximately 10% of paediatric posterior fossa tumours. Peak at 7 but range from 2-16 years old Well circumscribed Originate from floor or roof of 4th ventricle and extend into cerebellopontine angle, exiting from foramen of Luschka or Magendie More cellular than astrocytomas but less cellular than medulloblastoma, still demonstrating a great water content so on imaging: Hypodense on CT Low T1 High T2 Worse prognosis with: Incomplete resection Anaplastic histologically Ependymoma. (A to C) Axial T 2 , enhanced T 1 and coronal fluid-attenuated inversion recovery (FLAIR) images showing a solid and microcystic fourth ventricular tumour extending out through the foramina of Luschka, Magendie and the foramen magnum (arrows) , the typical features of an ependymoma. Cerebellar hemangioblastoma (WHO grade I) Ass with von Hippel–Lindau diseas. Sporadic form in adults. Rich capillary network. CT venography is optimal for major dural venous sinus thrombosis, whilst MRI/MRV is more likely to identify subtle parenchymal lesions and thrombosis of the smaller cortical veins. (A–C) This young male patient presented with headache and seizures. Serpiginous hyperdensity on computed tomography (CT) within a vessel on the surface of the right temporal lobe (A, black arrow ) and approaching the right lateral venous sinus (A and B, white arrows ) is consistent with the ‘string sign’ of cortical venous thrombosis—in this case, involving the right vein of Labbé. There is a small area of early venous ischaemia in the anterolateral aspect of the right temporal lobe on T 2 weighted (T 2 W) MRI (C, white arrow ). Lateral venous thrombosis. (D–J) A large acute parenchymal haemorrhage in the left frontal and temporal lobes was discovered on plain CT (D) in this patient who presented with seizures and encephalopathy. Hypointensity on the T 2 weighted magnetic resonance imaging (E) and susceptibility-weighted imaging (F) are consistent with acute blood products. There is a considerable degree of surrounding parenchymal oedema shown as high signal intensity on T 2 weighted. A causative left lateral sinus thrombosis is identified on T 2 weighted (G, white arrow ) and fluid-attenuated inversion recovery (H, white arrows ) with loss of the normal related signal void and confirmed by a filling defect within the left lateral sinus on the CT venogram (I, white arrow ; compare with right lateral sinus) and absence of flow-related signal in this sinus on magnetic resonance Cerebral venous thrombosis CVT / Sinus vein thrombosis SVT MRI / MRV better than CT to identify small thrombosis and parenchymal changes Missed on 40% of CTV Superficial cortical draining veins or deep draining dural venous sinuses Anticoagulation early – reduced venous drainage leads to venous hypertension and venous infarction that is often hemorrhagic infarction - SAH On MRI: low T2, low SWI signal due to hemosiderin – acute blood products Increased risk of SVT with: Osseous or air cell infection Trauma Dehydration Pregnancy OCP Smoking Vasculitis – especially Behcet Thrombophilia Deep cerebral veins more frequently than cortical veins Rarely cavernous sinus thrombosis – usually due to sinusitis/nasal sinus infection, dental infection, orbital infection On CT: hyperdense and expanded serpiginous structure hypodense center with enhancing periphery post-contrast – empty delta sign Delta sign on NCCT, empty delta sign on CTV / CECT Generally on MRI: loss of flow void on most sequences, can be high T1 and high T2/ high FLAIR signal – thrombosed vessel. Subacute thrombus / subacute SVT: high T1 and high T2 signal due to methemoglobin, expanded sinus - diagnostic DDx subacute hemorrhage has high T1 and high T2 signal due to methemoglobin Slow flow can mimic thrombus but slow flow is isointense on T1 and affects small segments On MRI SWI/on gradient echo: very low signal, expansion of the thrombosed vessel – blooming prominent serpiginous veins in the territory due to venous congestion 40% of children with SVT will have venous infarct Parenchymal complications of SVT Depend on whether there is venous hypertension, venous infarct or secondary hemorrhage Early there is disproportionate swelling and edema that are seen as on CT: hypodense On MRI: high T2/FLAIR with early fragmented hemorrhage Parenchymal lesions in affected areas correspond to the affected venous sinus, generally: Superior sagittal sinus thrombosis: parasagittal Internal cerebral vein thrombosis or straight sinus thrombosis or Vein of Galen – bilateral thalamus, basal ganglia Vein of Labbe thrombosis or transverse venous sinus thrombosis or sigmoid sinus thrombosis: temporal lobe posterolateral temporal lobe and inferior parietal lobule Vein of Labbé is one of the deep superficial venous system anastomoses connecting the middle cerebral vein to the transverse sinus Superior sagittal sinus thrombosis – bilateral cortical and subcortical lesions SAH often observed Cerebral venous infarct Can be due to SVT Do not conform to arterial territory – conform to venous territory Bilateral Frequently hemorrhagic infarcts On MRI DWI: mixture of restricted diffusion and free diffusion Congenital Lobar Overinflation -check valve mechanism Hyperinflation of the affected lobe. LUL, RML. immediate postnatal period may show a radio-opacity as the affected lobe is still full of fluid. CT will exclude other causes of secondary lobar overinflation: ascular anomalies, compression of the bronchi or mediastinal masses. conservative treatment and follow-up can show a reduction in overinflation Excision of the affected lobe is necessary in symptomatic children. Choledochal Malformation Abnormal widening of the biliary tract without obstruction. 80% in childhood, no malignant transformation. diameter greater than 4 mm suggests choledochal malformation Type V – Caroli disease – intrahepatic dilations (type V), hepatic fibrosis, cystic kidney disease Associated with hepatic fibrosis, ARPKD, medullary sponge kidney Can present as renal disease only A common pancreaticobiliary channel may be seen on US and with MRCP Flux of pancreatic excretions into the common bile duct is thought to be a pathogenetic factor The clinically most important DDx at the porta hepatic is cystic biliary atresia. Other differential diagnoses include duodenal duplication cyst and lymphangioma. Inspissated Bile partial or full obstruction by stagnant formed bile. Premature, hemolysis, functional obstruction (Hirschsprung) CF, total parenteral nutrition. US demonstrates the (slightly) echogenic bile with no acoustic shadowing, and the secondary biliary dilatation (mainly extrahepatic). There may be increased periportal echogenicity if long-standing.  Swyer-James-MacLeod syndrome post-infectious bronchiolitis obliterans post-adenovirus in childhood Unilateral Small branching centrilobular opacities, dilated peripheral bronchioles. In children, adenovirus may result in lobar collapse, especially of the right upper lobe.  Adenovirus infections in immunocompromised individuals, such as stem-cell and solid-organ transplant recipients, are increasingly recognized as significant causes of morbidity and mortality. In the stem-cell transplantation population, the incidence of disease ranges from 3% to 47%. he CT findings consist of patchy bilateral areas of consolidation in a lobular or segmental distribution and/or bilateral ground-glass opacities with a random distribution Bilateral cylindrical bronchiectasis: - the right upper and the lower lobes. -bronchial wall thickening. - mucoid impactions with slight volume loss of the right lower lobe. Note also a lung cyst in the posterior part of the right upper lobe. Cardinal sign – bronchial dilatation without tapering. Signet sigh – diameter of the bronchi more then artery. Bronchus us visible 1 cm from pleura. 70% associated bronchiolitis: centrilobular tree in bud. Mosaic perfusion, air trraping. (bronchiolitis obliterans). Note the multifocal air trapping on (D) perfectly matched with areas of low attenuation that reflect hypoperfusion due to hypoventilation secondary to obliterative bronchiolitis. (mosaic perfusion) on (C) well assessed by adapting the window width and window level. Atrial Situs Isomerism of the right atrial appendages AVSD – AV SEPTAL DEFECT Bilateral triilobed lung. Asplenia. Midline liver. Common AV junction ( instead two separate). AVSD – AV SEPTAL DEFECT. Gut malrotation. Isomerism of the left atrial appendages Bilateral bilobed lung. Polysplenia. IVC interuption. Ventricular Morphology The tricuspid valve is the direct attachments to the septum of cords from the septal leaflet. Unlike the tricuspid valve, the mitral valve has no direct septal attachments. The muscular structure of the ventricles also differs, with the RV being more trabeculated than the LV, with a muscular infundibulum and mid-ventricular ‘moderator band’. Congenital ureteropelvic junction (UPJ) obstruction screened by routine antenatal US intrinsic narrowing of the proximal ureter as it joins the renal pelvis (abberant of acsessory renal artery). Voiding cystourethrogram (VCUG) performed to assess for vesicoureteric reflux as a cause of hydronephrosis. Sturge-Weber Syndrome Fascial angioma Bilateral involvement may occasionally occur TRIGEMINAL DISTRIBUTION. Ipsilateral meningeal angiomatosis. tractable seizures, hemiparesis, hemianopsia and mental retardation. MRI findings:  pial angiomas in the parieto-occipital regions;  cortical calcifications subjacent to the cortex and white matter, typically in the parieto-occipital region;  enlarged choroid plexus;  atrophy of the ipsilateral cerebral hemisphere (angioma side);  enlarged and elongated globe of the eye; and  prominent enlarged subependymal and medullary veins, and secondary signs of cerebral atrophy involving the paranasal sinuses, mastoid cells and calvarium. leptomeningeal angiomas cause abnormal venous drainage with chronic ischaemia, leading ultimately to cortical atrophy and calcification. By 2 years of age, skull radiographs may reveal ‘tramline calcifications’ within the cortices. early imaging the brain may look normal on CT, as well as on MRI until after 2 years of life. Uncommon Bladder Neoplasms Squamous Cell Carcinomas: irritative neoplasm after UTI. Schistomiasis endemic. Adenocarcinoma Urachal carcinomas, bladder exstrophy, cystitis glandularis. Hematuria. Urachal transitional cell and squamous cell cancers and urachal sarcomas have also been encountered. Location – dome of the bladder. Hyper vascular component and cystic areas. Squamous Cell Carcinomas Bladder and Ureteric Metastases: melanoma. Magnetic Resonance Imaging of a Papillary Urothelial Neoplasm. (T2 and T1+). Known TCC of the bladder with involving of the ureter. Bladder cancers usually demonstrate brisk enhancement after gadolinium-based contrast material administration. Bladder injury: Usually from blunt trauma Only 2-10% of pelvic fractures have concurrent bladder injury Use CT cystography - performed in all patients with gross hematuria + pelvic fractures Better than fluoroscopy with 95% sensitivity and 99% specificity. Exception of isolated acetabular fracture After exclusion of urethral injury Instill at least 250ml to avoid false negatives 400ml of 4% can be instilled False negatives due to: contrast blocked by detrusor contraction, small tear, blood clots, Foley catheter Extraperitoneal bladder rupture Most common Due to bone spicules or pulling of fascia Anterolateral bladder and base On CT: molar tooth appearance Contrast into extraperitoneal tissues Disruption of urogenital diaphragm – posterior urethra- and bladder base Contrast extending into perineum and scrotum Conservative management – transurethral or suprapubic catheter drainage Intraperitoneal bladder rupture At weaker bladder dome When bladder is full More frequent in small children due to seatbelt Bladder higher Belt passes lower abdomen instead of superior iliac spines On CT: contrast outlines peritoneal recesses Appears less dense due to greater dilution Surgical management Extraperitoneal injury: anterior prevesical space of Retzius, the anterior abdominal wall, the inguinal regions and upper thigh, the lateral paravesical space and the presacral space. Intraperitoneal bladder injury demonstrates high-density fluid surrounding bowel loops. Blunt trauma most common.  Haematuria typically present.  Most patients will have concurrent pelvic fractures.  May be extraperitoneal rupture (most common), intraperitoneal rupture or mixed.  Computed tomography cystography required for accurate diagnosis.  Most EBRs managed conservatively (suprapubic or transurethral catheter)—90% healed in 10 days. IBRs usually require surgery. Nonaccidental Injury High specificity: Classic metaphyseal lesion Rib fractures, especially posterior Scapular fractures Spinous process fractures Sternal fractures Fractures of different ages Clavicular fractures Long bone shaft fractures Linear skull fractures Metaphyseal Injury CML Corner fracture’ (a thick rim only, arrowhead), ‘bucket handle’ (a thick rim projected away from the shaft, arrow) and a thin disk with a thick rim (stippled arrow). Imaging in Abusive Head Trauma US for initial CT – best first line. Subarachnoid hemorrhage (SAH) is better seen in the initial phase with CT than with conventional T1 and T2 WSE MRI, but FLAIR (hyperintensity) and SWI (hypointensity) are still sensitive. In young infants, SAH may be overdiagnosed on CT because the difference in density between the dura and parenchyma is higher than in the older child. Intraventricular hemorrhage may occur in the ‘shaken baby’ in connection with a subependymal venous injury and is easily detected on CT in the acute phase. On MRI, changes on T2* weighted or SWI sequences will remain for a while. Cranial ultrasound demonstrates a bilateral subdural haematoma (arrow) with compressed subarachnoid space (arrowhead) containing vessels between subdural spaces and brain. Doppler ultrasound shows a resistive index closed to 1, with any systolic flux indicating an intracranial hypertension \ 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 – ve